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The Raelian Movement
for those who are not afraid of the future : http://www.rael.org
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Cancer is DEAD: Cancer cured from A to Z
http://www.abovetopsecret.com/forum/cancerisdead.html
Topic started on 22-8-2010 @ 03:01 PM by IgnoranceIsntBlisss
Out of all of my media projects, I've never been more infuriated than
by this research thrust. You'd be hard-pressed to find someone that
wouldn't agree that the medical establishment isn't really trying to
cure cancer, and they're all correct.
The cure for cancer isn't one single silver bullet if only we could
find it (or they'd stop suppressing it). There are scores of cures for
cancer, and many of them all well known and out in the open, yet
nonpursued by probably the majority of the medical doctors or
industries out there. This presentation proves the beyond the shadow
of a doubt.
You'd think that the sorts of people in the business of saving lives,
especially those who deal in cancer 'treatments', would have a hobby
of reading the sorts of scholarly papers I dug through to compile
this. From there you'd think that from what they learn via this
hypothetical hobby they'd be constantly excited to tell their next
cancer patient about the latest simple and often natural remedies they
can also do themselves to have the best shot at surviving.
But the fact is this isn't how it works. In the wake of building this
presentation I've never been more convinced the the overarching
totality of the medical establishment are a massive group of
psychopaths. When they know about proven effective and safe
treatments, or are shown them by their patients, and they consciously
dismiss and shrug them off, how can these people not be deranged
sociopaths when their patients face horrifying death?
If you've ever witnessed the process of death via brain cancer for
instance, you'd catch my drift. I had an aunt die this way and it's
amongst the most disturbing ways you could ever contemplate your last
days on earth. Now my mom has lung cancer and they've pissed of the
wrong person. May their monopoly on suffering go crashing into the
abyss. Considering that about 550,000 people die annually from cancer,
I apologize to those for whom it's already too late, but I present to
you my most important presentation to date:
Cancer is DEAD: Cancer cured from A to Z
By Ignorance Isn't Bliss
ignoranceisfutile.org...
Acai Berries
Source: Fruits from the Açaí Palm.
en.wikipedia.org...
www.youtube.com...
Brazilian berry destroys cancer cells in lab, UF study shows
news.ufl.edu...
Published today in the Journal of Agricultural and Food Chemistry, the
study showed extracts from acai (ah-SAH'-ee) berries triggered a
self-destruct response in up to 86 percent of leukemia cells tested,
said Stephen Talcott, an assistant professor with UF's Institute of
Food and Agricultural Sciences. "Acai berries are already considered
one of the richest fruit sources of antioxidants," Talcott said. "This
study was an important step toward learning what people may gain from
using beverages, dietary supplements or other products made with the
berries."
Acrylamide (BAD)
www.cancer.gov...
*Acrylamide is a chemical used primarily for industrial purposes.
*Acrylamide has been found in certain foods, with especially high
levels in potato chips, French fries, and other food products produced
by high-temperature cooking.
*Food and cigarette smoke are the major sources of exposure to acrylamide.
*Acrylamide is considered to be a mutagen and a probable human
carcinogen, based mainly on studies in laboratory animals.
*Scientists do not yet know with any certainty whether the levels of
acrylamide typically found in some foods pose a health
risk for humans.
How does cooking produce acrylamide?
Asparagine is an amino acid (a building block of proteins) that is
found in many vegetables, with higher concentrations in some varieties
of potatoes. When heated to high temperatures in the presence of
certain sugars, asparagine can form acrylamide. High-temperature
cooking methods, such as frying, baking, or broiling, have been found
to produce acrylamide (3), while boiling and microwaving appear less
likely to do so. Longer cooking times can also increase acrylamide
production when the cooking temperature is above 120 degrees Celsius
(4, 5).
Aloe-emodin
Sources: Aloe Vera Plant, Aloe Vera Juice (inexpensive at Hispanic Markets).
Aloe-Emodin Induces Apoptosis in T24 Human Bladder Cancer Cells
www.ncbi.nlm.nih.gov...
AE inhibited cell viability, and induced G2/M arrest and apoptosis in
T24 cells. AE increased the levels of Wee1 and cdc25c, and may have
led to inhibition of the levels of cyclin-dependent kinase 1 and
cyclin B1, which cause G2/M arrest. AE induced p53 expression and was
accompanied by the induction of p21 and caspase-3 activation, which
was associated with apoptosis. In addition, AE was associated with a
marked increase in Fas/APO1 receptor and Bax expression but it
inhibited Bcl-2 expression.
Protein kinase C involvement in aloe-emodin- and emodin-induced
apoptosis in lung carcinoma cell
www.ncbi.nlm.nih.gov...
This study demonstrated aloe-emodin- and emodin-induced apoptosis in
lung carcinoma cell lines CH27 (human lung squamous carcinoma cell)
and H460 (human lung non-small cell carcinoma cell). Aloe-emodin- and
emodin-induced apoptosis was characterized by nuclear morphological
changes and DNA fragmentation.
The antiproliferative activity of aloe-emodin is through p53-dependent
and p21-dependent apoptotic pathway in human hepatoma cell lines
www.ncbi.nlm.nih.gov...
The aim of this study is to investigate the anticancer effect of
aloe-emodin in two human liver cancer cell lines, Hep G2 and Hep 3B.
We observed that aloe-emodin inhibited cell proliferation and induced
apoptosis in both examined cell lines, but with different the
antiproliferative mechanisms.
Aloe-emodin Is a New Type of Anticancer Agent with Selective Activity
against Neuroectodermal Tumors
cancerres.aacrjournals.org...
Here we report that aloe-emodin (AE), a hydroxyanthraquinone present
in Aloe vera leaves, has a specific in vitro and in vivo
antineuroectodermal tumor activity. The growth of human
neuroectodermal tumors is inhibited in mice with severe combined
immunodeficiency without any appreciable toxic effects on the animals.
The compound does not inhibit the proliferation of normal fibroblasts
nor that of hemopoietic progenitor cells. The cytotoxicity mechanism
consists of the induction of apoptosis, whereas the selectivity
against neuroectodermal tumor cells is founded on a specific
energy-dependent pathway of drug incorporation. Taking into account
its unique cytotoxicity profile and mode of action, AE might represent
a conceptually new lead antitumor drug.
Aloe-emodin induced in vitro G2/M arrest of cell cycle in human
promyelocytic leukemia HL-60 cells
www.ncbi.nlm.nih.gov...
Aloe-emodin inhibited cell proliferation and induced G2/M arrest and
apoptosis in HL-60 cells. Investigation of the levels of cyclins B1, E
and A by immunoblot analysis showed that cyclin E level was
unaffected, whereas cyclin B1 and A levels increased with aloe-emodin
in HL-60 cells. Investigation of the levels of cyclin-dependent
kinases, Cdk1 and 2, showed increased levels of Cdk1 but the levels of
Cdk2 were not effected with aloe-emodin in HL-60 cells. The levels of
p27 were increased after HL-60 cells were cotreated with various
concentrations of aloe-emodin.
Aloe-emodin-induced apoptosis in human gastric carcinoma cells
www.ncbi.nlm.nih.gov...
The purpose of this study was to investigate the anticancer effect of
aloe-emodin, an anthraquinone compound present in the leaves of Aloe
vera, on two distinct human gastric carcinoma cell lines, AGS and
NCI-N87. We demonstrate that aloe-emodin induced cell death in a dose-
and time-dependent manner. Noteworthy is that the AGS cells were
generally more sensitive than the NCI-N87 cells. Aloe-emodin caused
the release of apoptosis-inducing factor and cytochrome c from
mitochondria, followed by the activation of caspase-3, leading to
nuclear shrinkage and apoptosis.
[edit on 22-8-2010 by IgnoranceIsntBlisss]
reply posted on 22-8-2010 @ 03:06 PM by IgnoranceIsntBlisss
Aloe-emodin induces in vitro G2/M arrest and alkaline phosphatase
activation in human oral cancer KB cells
www.ncbi.nlm.nih.gov...
Aloe-emodin is a natural anthraquinone compound from the root and
rhizome of Rheum palmatum. In this study, KB cells were treated with
2.5, 5, 10, 20, and 40 microM aloe-emodin for 1 to 5 days. The results
showed that aloe-emodin inhibited cancer cells in a dose-dependent
manner. Treatment with aloe-emodin at 10 to 40 microM resulted in cell
cycle arrest at G2/M phase. The alkaline phosphatase (ALP) activity in
KB cells increased upon treatment with aloe-emodin when compared to
controls. This is one of the first studies to focus on the expression
of ALP in human oral carcinomas cells treated with aloe-emodin. These
results indicate that aloe-emodin has anti-cancer effect on oral
cancer, which may lead to its use in chemotherapy and chemopreventment
of oral cancer.
Anandamide
Source: Cannabis
www.ncbi.nlm.nih.gov...
The endogenous cannabinoid anandamide inhibits human breast cancer
cell proliferation
www.ncbi.nlm.nih.gov...
Anandamide was the first brain metabolite shown to act as a ligand of
"central" CB1 cannabinoid receptors. Here we report that the
endogenous cannabinoid potently and selectively inhibits the
proliferation of human breast cancer cells in vitro. Anandamide
dose-dependently inhibited the proliferation of MCF-7 and EFM-19 cells
with IC50 values between 0.5 and 1.5 μM and 83–92% maximal inhibition
at 5–10 μM. The proliferation of several other nonmammary tumoral cell
lines was not affected by 10 μM anandamide. The anti-proliferative
effect of anandamide was not due to toxicity or to apoptosis of cells
but was accompanied by a reduction of cells in the S phase of the cell
cycle. ...These data suggest that anandamide blocks human breast
cancer cell proliferation through CB1-like receptor-mediated
inhibition of endogenous prolactin action at the level of prolactin
receptor.
Anti-proliferative and apoptotic effects of anandamide in human
prostatic cancer cell lines
onlinelibrary.wiley.com...
ANA induced a decrease of EGFR levels on LNCaP, DU145, and PC3
prostatic cancer cells by acting through cannabinoid CB1 receptor
subtype and this leaded to an inhibition of the EGF-stimulated growth
of these cells. Moreover, the G1 arrest of metastatic DU145 and PC3
growth was accompanied by a massive cell death by apoptosis and/or
necrosis while LNCaP cells were less sensitive to cytotoxic effects of
ANA. The apoptotic/necrotic responses induced by ANA on these
prostatic cancer cells were also potentiated by the acidic ceramidase
inhibitor, N-oleoylethanolamine and partially inhibited by the
specific ceramide synthetase inhibitor, fumonisin B1 indicating that
these cytotoxic actions of ANA might be induced via the cellular
ceramide production. The potent anti-proliferative and cytotoxic
effects of ANA on metastatic prostatic cancer cells might provide
basis for the design of new therapeutic agents for effective treatment
of recurrent and invasive prostatic cancers.
Anandamide is an endogenous inhibitor for the migration of tumor cells
and T lymphocytes
www.springerlink.com...
Cell migration is of paramount importance in physiological processes
such as immune surveillance, but also in the pathological processes of
tumor cell migration and metastasis development. The factors that
regulate this tumor cell migration, most prominently
neurotransmitters, have thus been the focus of intense investigation.
While the majority of neurotransmitters have a stimulatory effect on
cell migration, we herein report the inhibitory effect of the
endogenous substance anandamide on both tumor cell and lymphocyte
migration. ...Using the specific agonist docosatetraenoylethanolamide
(DEA), we have observed that the norepinephrine-induced migration of
colon carcinoma cells is inhibited by the CB1-R. The SDF-1–induced
migration of CD8+ T lymphocytes was, however, inhibited via the CB2-R,
as shown by using the specific agonist JWH 133. Therefore, specific
inhibition of tumor cell migration via CB1-R engagement might be a
selective tool to prevent metastasis formation without depreciatory
effects on the immune system of cancer patients.
The endogenous cannabinoid, anandamide, induces cell death in
colorectal carcinoma cells
gut.bmj.com...
These findings suggest anandamide may be a useful
chemopreventive/therapeutic agent for colorectal cancer as it targets
cells that are high expressors of COX-2, and may also be used in the
eradication of tumour cells that have become resistant to apoptosis.
Apigenin
Foods: Parsley, Celery, Coriander, Licorice, Majoram, Oregano,
Rosemary, Tarragon, Citrus, Tea and Wheat.
en.wikipedia.org...
Selective growth-inhibitory, cell-cycle deregulatory and apoptotic
response of apigenin in normal versus human prostate carcinoma cells
www.ncbi.nlm.nih.gov...
The growth-inhibitory and apoptotic potential of apigenin was also
observed in a variety of prostate carcinoma cells representing
different stage and androgen responsiveness. Apigenin may be developed
as a promising chemopreventive and/or chemotherapeutic agent against
prostate cancer.
Apigenin induces apoptosis...in breast cancer cells
www.ncbi.nlm.nih.gov...
Apigenin is a low toxicity and non-mutagenic phytopolyphenol and
protein kinase inhibitor. It exhibits anti-proliferating effects on
human breast cancer cells. Here we examined several human breast
cancer cell lines having different levels of HER2/neu expression and
found that apigenin exhibited potent growth-inhibitory activity in
HER2/neu-overexpressing breast cancer cells but was much less
effective for those cells expressing basal levels of HER2/neu.
Signal pathways involved in apigenin inhibition of growth and
induction of apoptosis of human anaplastic thyroid cancer cells
www.ncbi.nlm.nih.gov...
Recently we demonstrated that several flavonoids can inhibit the
proliferation of certain human thyroid cancer cell lines. Among the
flavonoids tested, apigenin and luteolin are the most effective
inhibitors of these tumor cell lines. In the present study, we
investigated the signal transduction mechanism associated with the
growth inhibitory effect of apigenin, using a human anaplastic thyroid
carcinoma cell line, ARO.
Induction of cell cycle arrest and apoptosis by apigenin in human
prostate carcinoma cells
www.ncbi.nlm.nih.gov...
Apigenin, a common dietary flavonoid abundantly present in fruits and
vegetables, may have the potential for prevention and therapy for
prostate cancer. Here, we report for the first time that apigenin
inhibits the growth of androgen-responsive human prostate carcinoma
LNCaP cells and provide molecular understanding of this effect.
Induction of apoptosis by apigenin in leukaemia HL-60 cells
www.ejcancer.info...(99)00168-9/abstract
The potency of these flavonoids on these features of apoptosis were in
the order of: apigenin>quercetin>myricetin>kaempferol in HL-60 cells
treated with 60μM flavonoids. These results suggest that
flavonoid-induced apoptosis is stimulated by the release of cytochrome
c to the cytosol, by procaspase-9 processing, and through a
caspase-3-dependent mechanism. The induction of apoptosis by
flavonoids may be attributed to their cancer chemopreventive activity.
Furthermore, the potency of flavonoids for inducing apoptosis may be
dependent on the numbers of hydroxyl groups in the 2-phenyl group and
on the absence of the 3-hydroxyl group. This provides new information
on the structure–activity relationship of flavonoids.
5,6-Dichloro-ribifuranosylbenzimidazole- and apigenin-induced
sensitization of colon cancer cells to TNF--mediated apoptosis
ajpgi.physiology.org...
Here we report that inhibition of CK2 in HCT-116 and HT-29 cells with
the use of two specific CK2 inhibitors,
5,6-dichloro-ribifuranosylbenzimidazole (DRB) and apigenin, effected a
synergistic reduction in cell survival when used in conjunction with
TNF-. Furthermore, there was a demonstrable synergistic reduction in
colony formation in soft agar with the use of the same combinations.
Apoptosis
en.wikipedia.org...
Apoptosis (aka Programmed Cell Death) is the internal mechanism of
basically all biological cells to self-destruct when 'malfunctioning'.
With cancer cells mutate and overcome this design, making them in a
sense immortal. So for about as long as cancer has been understood the
holy grail in cancer research has been in discovering how to
reinstitute apoptosis in cancer cells safely.
[edit on 22-8-2010 by IgnoranceIsntBlisss]
copyright & usage
reply posted on 22-8-2010 @ 03:08 PM by IgnoranceIsntBlisss
The thing is this holy grail has been found in numerous forms, yet the
understanding of the general public is that it hasn't and can only be
solved with damaging radiation and chemotherapy. You might ask
yourself why that is, and why haven't known safe apoptosis inducers
been aggressively pursued? Perhaps preventing terrorist attacks on
national monuments are more important than the 550,000 individuals who
die every year from cancer?
Arachidonyl Ethanolamide
Source: Cannabis
Arachidonyl ethanolamide induces apoptosis of uterine cervix cancer
cells via aberrantly expressed vanilloid receptor-1
www.ncbi.nlm.nih.gov...
The major finding was that AEA induced apoptosis of CxCa cell lines
via aberrantly expressed vanilloid receptor-1, whereas AEA binding to
the classical CB1 and CB2 cannabinoid receptors mediated a protective
effect. Furthermore, unexpectedly, a strong expression of the three
forms of AEA receptors was observed in ex vivo CxCa biopsies.
Artemisinin
Source: Wormwood Plant
en.wikipedia.org...
Artemisinin Induces Apoptosis in Human Cancer Cells
ar.iiarjournals.org...
Artemisinin is a chemical compound extracted from the wormwood plant,
Artemisia annua L. It has been shown to selectively kill cancer cells
in vitro and retard the growth of implanted fibrosarcoma tumors in
rats. In the present research, we investigated its mechanism of
cytotoxicity to cancer cells. ...This rapid induction of apoptosis in
cancer cells after treatment with DHA indicates that artemisinin and
its analogs may be inexpensive and effective cancer agents.
Effects of artemisinin and its derivatives on growth inhibition and
apoptosis of oral cancer cells
onlinelibrary.wiley.com...
Artemisinin is of special biological interest because of its
outstanding antimalarial activity. Recently, it was reported that
artemisinin has antitumor activity. Its derivatives, artesunate,
arteether, and artemeter, also have antitumor activity against
melanoma, breast, ovarian, prostate, CNS, and renal cancer cell lines.
Recently, monomer, dimer, and trimer derivatives were synthesized from
deoxoartemisinin, and the dimers and the trimers were found to have
much more potent antitumor activity than the monomers. ...The
deoxoartemisinin trimer was found to have greater antitumor effect on
tumor cells than other commonly used chemotherapeutic drugs, such as
5-FU, cisplatin, and paclitaxel. Furthermore, the ability of
artemisinin and its derivatives to induce apoptosis highlights their
potential as chemotherapeutic agents, for many anticancer drugs
achieve their antitumor effects by inducing apoptosis in tumor cells.
Transferrin receptor-dependent cytotoxicity of artemisinin–transferrin
conjugates on prostate cancer cells and induction of apoptosis
www.ncbi.nlm.nih.gov...
Artemisinin, a natural product isolated from Artemisia annua, contains
an endoperoxide group that can be activated by intracellular iron to
generate toxic radical species. Cancer cells over-express transferrin
receptors (TfR) for iron uptake while most normal cells express nearly
undetectable levels of TfR. We prepared a series of artemisinin-tagged
transferrins (ART-Tf) where different numbers of artemisinin units are
attached to the N-glycoside chains of transferrin (Tf). The Tf bearing
approximately 16 artemisinins retains the functionality of both Tf and
artemisinin. Reduction of TfRs by TfR siRNA transfection significantly
impaired the ability of ART-Tf, but not dihydroartemisinin, to kill
cells. We also demonstrate that the ART-Tf conjugate kills the
prostate carcinoma cell line DU 145 by the mitochondrial pathway of
apoptosis.
Transferrin overcomes drug resistance to artemisinin in human
small-cell lung carcinoma cells
www.cancerletters.info...(02)00005-8/abstract
Multiple drug resistance is a significant problem in small-cell lung
cancer (SCLC). Artemisinin (ART) is a natural product used to treat
drug-resistant malaria. The drug is effective because the Fe2+ present
in infected erythrocytes acts non-enzymatically to convert ART to
toxic products. We tested the effects of ART on drug-sensitive (H69)
and multi-drug-resistant (H69VP) SCLC cells, pretreated with
transferrin (TF) to increase the intracellular Fe2+ level. ...These
data indicate the potential use of ART and TF in drug-resistant SCLC.
Dihydroartemisinin induces apoptosis and sensitizes human ovarian
cancer cells to carboplatin therapy
www.ncbi.nlm.nih.gov...
The present study was designed to determine the effects of artemisinin
(ARS) and its derivatives on human ovarian cancer cells, to evaluate
their potential as novel chemotherapeutic agents used alone or in
combination with a conventional cancer chemotherapeutic agent, and to
investigate their underlying mechanisms of action. Human ovarian
cancer cells (A2780 and OVCAR-3), and immortalized non-tumourigenic
human ovarian surface epithelial cells (IOSE144), were exposed to four
ARS compounds for cytotoxicity testing. The in vitro and in vivo
antitumour effects and possible underlying mechanisms of action of
dihydroartemisinin (DHA), the most effective compound, were further
determined in ovarian cancer cells. ...These effects were also
observed in in vivo ovarian A2780 and OVCAR-3 xenograft tumour models.
In conclusion, ARS derivatives, particularly DHA, exhibit significant
anticancer activity against ovarian cancer cells in vitro and in vivo,
with minimal toxicity to non-tumourigenic human OSE cells, indicating
that they may be promising therapeutic agents for ovarian cancer,
either used alone or in combination with conventional chemotherapy.
β-Elemene
Source: Ginger Root
en.wikipedia.org...
Antitumor effect of β-elemene in non-small-cell lung cancer cells is
mediated via induction of cell cycle arrest and apoptotic cell death
www.springerlink.com...
Beta-elemene is a novel anticancer drug, which was extracted from the
ginger plant. However, the mechanism of action of beta-elemene in
non-small-cell lung cancer (NSCLC) remains unknown. Here we show that
beta-elemene had differential inhibitory effects on cell growth
between NSCLC cell lines and lung fibroblast and bronchial epithelial
cell lines. ...These data indicate that the effect of beta-elemene on
lung cancer cell death may be through a mitochondrial release of the
cytochrome c-mediated apoptotic pathway.
Elemene displays anti-cancer ability on laryngeal cancer cells in
vitro and in vivo
www.springerlink.com...
Elemene inhibited the growth of HEp-2 cells in vitro in a dose- and
time-dependent manner with an IC50 of 346.5 μM (24 h incubation).
Increased apoptosis was observed in elemene-administered cells.
Elemene is suspected to enhance caspase-3 activity, and thus inhibit
protein expression of eIFs (4E, 4G), bFGF, and VEGF. In vivo, the
growth of HEp-2 cell-transplanted tumors in nude mice was inhibited by
intraperitoneal injection of elemene. Compared with control groups,
elemene significantly inhibited the protein expression of eIFs (4E and
4G), bFGF, and VEGF and decreased the MVD. Conclusions: Elemene
inhibits the growth of HEp-2 cells in vitro and in vivo. These data
provide useful information for further clinical study on the treatment
of LSCC by elemene.
Antiproliferative effect of β-elemene in chemoresistant ovarian carcinoma cells
www.springerlink.com...
In this study, we show that beta-elemene inhibited the proliferation
of cisplatin-resistant human ovarian cancer cells and their parental
cells, but had only a marginal effect in human ovary cells, indicating
differential inhibitory effects on cell growth between ovarian cancer
cells and normal ovary cells.
Effect of Local Arterial Infusion of β_elemene on Breast Cancer Tissue
Inhibition and Cell Apoptosis and Proliferation
en.cnki.com.cn...
The effect of local arterial infusion of β_elemene on breast cancer
tissue inhibition and cell apoptosis and proliferation was observed.
N-(beta-Elemene-13-yl)tryptophan methyl ester induces apoptosis in
human leukemia cells
www.ncbi.nlm.nih.gov...
Beta-elemene is an active component of herb medicine Curcuma Wenyujin
and N-(beta-elemene-13-yl)tryptophan methyl ester (ETME) was
synthesized for increasing its antitumor activity. ETME induced
apoptosis in human leukemia HL-60 and NB4 cells at concentrations less
than 40 microM. The apoptosis induction ability of ETME was associated
with the production of hydrogen peroxide (H(2)O(2)), the decrease of
mitochondrial membrane potential, and the activation of caspase-3 that
was blocked by catalase. ETME in combination with arsenic trioxide
(As(2)O(3)), an agent used to treat acute promyelocytic leukemia,
synergistically induced apoptosis in both cell lines by enhanced
production of H(2)O(2). These data suggest that ETME induces apoptosis
and synergizes with As(2)O(3) in leukemia cells through a
H(2)O(2)-dependent pathway.
copyright & usage
reply posted on 22-8-2010 @ 03:10 PM by IgnoranceIsntBlisss
ß-Glucan
Foods: Mushrooms, Grains & Yeast.
Mushrooms: Shiitake (Lentinula edodes), Reishi (Ganoderma lucidum &
Ganoderma tsugae), Maitake (Grifola frondosa), Oyster Mushroom
(Pleurotus ostreatus), Cauliflower Mushroom (Sparassis).
Grains: Oats, Barley.
Fights cancer and eases the effects of radiation.
NOTE: Literally all of the listed mushrooms above have other important
anti-cancer effects not necessarily specified by this presentation.
ß-Glucan...Uses Antibodies to Target Tumors for Cytotoxic Recognition
by Leukocyte Complement Receptor Type 3 (CD11b/CD18)
www.jimmunol.org...
ß-Glucans were identified 36 years ago as a biologic response modifier
that stimulated tumor rejection. In vitro studies have shown that
ß-glucans bind to a lectin domain within complement receptor type 3
(CR3; known also as Mac-1, CD11b/CD18, or Mß2-integrin, that functions
as an adhesion molecule and a receptor for factor I-cleaved C3b, i.e.,
iC3b) resulting in the priming of this iC3b receptor for cytotoxicity
of iC3b-opsonized target cells. This investigation explored mechanisms
of tumor therapy with soluble ß-glucan in mice. Normal mouse sera were
shown to contain low levels of Abs reactive with syngeneic or
allogeneic tumor lines that activated complement, depositing C3 onto
tumors. Implanted tumors became coated with IgM, IgG, and C3, and the
absent C3 deposition on tumors in SCID mice was reconstituted with IgM
or IgG isolated from normal sera. Therapy of mice with glucan- or
mannan-rich soluble polysaccharides exhibiting high affinity for CR3
caused a 57–90% reduction in tumor weight. In young mice with lower
levels of tumor-reactive Abs, the effectiveness of ß-glucan was
enhanced by administration of a tumor-specific mAb, and in SCID mice,
an absent response to ß-glucan was reconstituted with normal IgM or
IgG. The requirement for C3 on tumors and CR3 on leukocytes was
highlighted by therapy failures in C3- or CR3-deficient mice. Thus,
the tumoricidal function of CR3-binding polysaccharides such as
ß-glucan in vivo is defined by natural and elicited Abs that direct
iC3b deposition onto neoplastic cells, making them targets for
circulating leukocytes bearing polysaccharide-primed CR3. Therapy
fails when tumors lack iC3b, but can be restored by tumor-specific Abs
that deposit iC3b onto the tumors.
Beta glucan induces proliferation and activation of monocytes in
peripheral blood of patients with advanced breast cancer
www.ncbi.nlm.nih.gov...
Glucans are glucose polymers that constitute a structural part of
fungal cell wall. They can stimulate the innate immunity by activation
of monocytes/macrophages. In human studies it has been shown that beta
glucan has an immunomodulatory effect and can increase the efficacy of
the biological therapies in cancer patients. In this prospective
clinical trial we assessed in vivo effects of short term oral beta
glucan administration on peripheral blood monocytes and their
expression of activation markers in patients with advanced breast
cancer. ...Oral beta glucan administration seems to stimulate
proliferation and activation of peripheral blood monocytes in vivo in
patients with advanced breast cancer.
Yeast ß-Glucan Amplifies Phagocyte Killing of iC3b-Opsonized Tumor Cells
www.jimmunol.org...
Anti-tumor mAbs hold promise for cancer therapy, but are relatively
inefficient. Therefore, there is a need for agents that might amplify
the effectiveness of these mAbs. One such agent is -glucan, a
polysaccharide produced by fungi, yeast, and grains, but not mammalian
cells. -Glucans are bound by C receptor 3 (CR3) and, in concert with
target-associated complement fragment iC3b, elicit phagocytosis and
killing of yeast. -Glucans may also promote killing of iC3b-opsonized
tumor cells engendered by administration of anti-tumor mAbs. In this
study, we report that tumor-bearing mice treated with a combination of
-glucan and an anti-tumor mAb show almost complete cessation of tumor
growth.
Chemosensitization of Carmustine with Maitake β-Glucan on
Androgen-Independent Prostatic Cancer Cells
www.liebertonline.com...
This study demonstrates a sensitized cytotoxic effect of BCNU with
β-glucan in PC-3 cells, which was associated with a drastic (~80%)
inactivation of Gly-I. Therefore, the BCNU/β-glucan combination may
help to improve current treatment efficacy by targeting Gly-I, which
appears to be critically involved in prostate cancer viability.
ß-Hydroxyisovalerylshikonin
Source: Lithospermum (herbs).
www.wikigenes.org...
ß-Hydroxyisovalerylshikonin Inhibits the Cell Growth of Various Cancer
Cell Lines and Induces Apoptosis in Leukemia HL–60 Cells
jb.oxfordjournals.org...
ß-Hydroxyisovalerylshikonin (ß-HIVS), which was isolated from the
plant, Lithosper-mium radix, inhibited the growth of various lines of
cancer cells derived from human solid, tumors at low concentrations
between 10-8 and 10-6 M. When HL-60 cells were treated with 10-6 M
ß-HIVS for 3 h, characteristic features of apoptosis, such as DNA
fragmentation, nuclear fragmentation, and activation of caspase-3–like
activity, were observed.
β-Hydroxyisovalerylshikonin and Cisplatin Act Synergistically to
Inhibit Growth and to Induce Apoptosis of Human Lung Cancer DMS114
Cells
www.ncbi.nlm.nih.gov...
beta-Hydroxyisovalerylshikonin (beta-HIVS) and cisplatin (CDDP) had a
synergistic growth-inhibitory effect on cultured human small-cell lung
carcinoma DMS114 cells, as well as on human leukemia U937 and
epidermoid carcinoma A431 cells, while beta-HIVS and CDDP alone at the
same respective concentrations had little effect.
Betulin
Source: The bark of Red Alder trees & White Birch trees, and the
mushroom Chaga that grows on White Birch.
en.wikipedia.org...
Anti-Cancer Effect of Betulin on a Human Lung Cancer Cell Line
www.thieme-connect.com...
Betulin is a representative compound of Betula platyphylla, a tree
species belonging to the Betulaceae family. In this investigation, we
revealed that betulin showed anticancer activity on human lung cancer
A549 cells by inducing apoptosis and changes in protein expression
profiles were observed.
Betulinic Acid Inhibits Prostate Cancer Growth
cancerres.aacrjournals.org...
Betulinic acid is a pentacyclic triterpene natural product initially
identified as a melanoma-specific cytotoxic agent that exhibits low
toxicity in animal models. Subsequent studies show that betulinic acid
induces apoptosis and antiangiogenic responses in tumors derived from
multiple tissues;
Apoptotic activity of betulinic acid derivatives on murine melanoma
B16 cell line
www.ncbi.nlm.nih.gov...
Exposure of B16 cells to betulinic acid, 23-hydroxybetulinic acid and
3-oxo-23-hydroxybetulinic acid caused a rapid increase in reactive
oxidative species production and a concomitant dissipation of
mitochondrial membrane potential in a dose- and time-dependent manner,
which resulted in cell apoptosis, as demonstrated by fluorescence
microscopy, gel electrophoresis and flow-cytometric analysis. Cell
cycle analysis further demonstrated that both
3-oxo-23-hydroxybetulinic acid and 23-hydroxybetulinic acid
dramatically increased DNA fragmentation at the expense of G1 cells at
doses as low as 12.5 and 25 microg/ml, respectively, thereby showing
their potent apoptotic properties. Our results showed that
hydroxylation at the C3 position of betulinic acid is likely to
enhance the apoptotic activity of betulinic acid derivatives
(23-hydroxybetulinic acid and 3-oxo-23-hydroxybetulinic acid) on
murine melanoma B16 cells.
Betulinic acid induces apoptosis in human neuroblastoma cell lines
www.ncbi.nlm.nih.gov...
Neuroblastoma has long been recognized to show spontaneous regression
during fetal development and in the majority of stage 4s infants <1
year of age with disseminated disease. Stage 4s disease regresses with
no chemotherapy in 50% of the patients. The mechanism by which this
occurs is not understood but may be programmed cell death or
apoptosis. Betulinic acid (BA) has been reported to induce apoptosis
in human melanoma with in vitro and in vivo model systems.
Betulinic acid induces apoptosis in skin cancer cells
onlinelibrary.wiley.com...
Betulinic acid (BA), a pentacyclic triterpene of plant origin, induces
cell death in melanoma cells and other malignant cells of
neuroectodermal origin. Little is known about additional biological
effects in normal target cells. We show, in this study, that BA
induces differentiation as well as cell death in normal human
keratinocytes (NHK).
copyright & usage
AboveTopSecret.com is advertising supported.
reply posted on 22-8-2010 @ 03:11 PM by IgnoranceIsntBlisss
Betulinic acid: A new cytotoxic compound against malignant head and
neck cancer cells
onlinelibrary.wiley.com...
In two HNSCC cell lines betulinic acid induced apoptosis, which was
characterized by a dose-dependent reduction in cell numbers, emergence
of apoptotic cells, and an increase in caspase activity. Western blot
analysis of the expression of various Bcl-2 family members in
betulinic acid–treated cells showed, surprisingly, a suppression of
the expression of the proapoptotic protein Bax but no changes in Mcl-1
or Bcl-2 expression.
In vivo and in vitro anti-inflammatory and anti-nociceptive effects of
the methanol extract of Inonotus obliquus
www.ncbi.nlm.nih.gov...
The mushroom Inonotus obliquus (Fr.) Pilát (Hymenochaetaceae), has
been traditionally used for the treatment of gastrointestinal cancer,
cardiovascular disease and diabetes in Russia, Poland and most of
Baltic countries. This study was designed to investigate the
anti-inflammatory and anti-nociceptive effects of the methanol extract
from Inonotus obliquus (MEIO) in vivo and in vitro. MEIO (100 or 200
mg/(kg day), p.o.) reduced acute paw edema induced by carrageenin in
rats, and showed analgesic activity, as determined by an acetic
acid-induced abdominal constriction test and a hot plate test in mice.
Blueberries
en.wikipedia.org...
Effect of Anthocyanin Fractions from Selected Cultivars of
Georgia-Grown Blueberries on Apoptosis and Phase II Enzymes
pubs.acs.org...
The response correlated positively with dose. The QR activity was
lower in all cells treated with an anthocyanin fraction from Tifblue,
Powderblue, Brightblue, and Brightwell cultivars than in control cells
(P < 0.05). The activity decreased gradually when treated with
increased concentrations of anthocyanin fractions (50−150 μg/mL) in
the Tifblue and Powderblue cultivars. The GST activity was lower (P <
0.05) in cells treated with anthocyanin fractions from all of the
cultivars and at all concentrations. These results indicated that
apoptosis was confirmed in HT-29 cells when treated with anthocyanins
from blueberry cultivars at 50−150 μg/mL concentrations, but these
same concentrations decrease QR and GST activities rather than induce
them.
Availability of blueberry phenolics for microbial metabolism in the
colon and the potential inflammatory implications
www.ncbi.nlm.nih.gov...
Blueberries are a rich source of phenylpropanoid-derived
phytochemicals, widely studied for their potential health benefits. Of
particular interest for colonic health are the lower molecular weight
phenolic acids and their derivatives, as these are the predominant
phenolic compounds detected in the colon. Blueberries contained a wide
variety of phenolic acids, the majority of which (3371.14 ± 422.30
mg/kg compared to 205.06 ± 45.34 mg/kg for the free phenolic acids)
were attached to other plant cell-wall components and therefore,
likely to become available in the colon. Cytokine-induced stimulation
of the inflammatory pathways in colon cells was four-fold up-regulated
in the presence of the free phenolic acid fraction. Incubation of the
bound phenolic acids with human faecal slurries resulted in
qualitative and quantitative differences in the phenolic compounds
recovered. The metabolites obtained by incubation with faecal slurries
from one volunteer significantly decreased (1.67 ± 0.69 ng/cm3)
prostanoid production, whereas an increase (10.78 ± 5.54 ng/cm3) was
obtained with faecal slurries from another volunteer. These results
suggest that any potential protective effect of blueberry phenolics as
anti-inflammatory agents in the colon is a likely result of microbial
metabolism. Studies addressing a wide-range of well-characterised
human volunteers will be required before such health claims can be
fully established.
Broccoli
Relatives: Romanesco, Broccoflower, Cauliflower, Kale, Raab, Brussel
Sprouts, Cabbage, Collards and Kohl Rabi.
en.wikipedia.org...
Don't boil!
Natural Compound in Broccoli Slows Breast Cancer Stem Cells
breastcancer.about.com...
In lab studies, when breast cancer cells were exposed to sulforaphane
extract from broccoli, the growth of cancer stems cells slowed down
and tumors shrank. The researchers speculate about the possible use of
sulforaphane extract to prevent as well as treat breast cancer,
someday.
Sprouts contain 3X the amount of Sulforaphane Glucosinolate
www.broccosprouts.com...
Johns Hopkins University researchers found that young broccoli
sprouts, in particular, contained high concentrations of SGS.
The scientists believe that SGS boosts the body's own antioxidant
defense system, including Phase 2 detoxification enzymes, which
promote long-lasting antioxidant activity in the body.
Diindolylmethane (DIM)
www.activamune.com...
At the University of California at Berkeley, the Chairman of the
Nutritional Sciences Department and the Director of the National
Institutes of Health Cancer Research Program were studying the
biological properties of Diindolylmethane (DIM), a naturally occurring
compound found in Brassica vegetables (broccoli, cauliflower, cabbage,
kale, brussels sprouts), when they made a remarkable discovery: DIM is
a potent activator of the immune response system. They patented their
discovery and ActivaMune was launched as a first-in-class nutritional
supplement to enhance the immune system and support multiple organs
throughout the body: breast, prostate, cardiovascular, vision, skin
and colon health. ActivaMune's unique and patented formula combines
multiple nutrients for maximum effectiveness: Diindolylmethane (DIM),
Sulforaphane, Selenium, Lycopene, Lutein, Zeaxanthin, Calcium and
Vitamins C, D3 & E.
Butyric Acid
en.wikipedia.org...
This is formed naturally during the digestion of dietary fibers. Not
enough BA and you're prone to colon cancer. If you get colon cancer
you it's time to go into fiber overdrive.
onlinelibrary.wiley.com...
Caffeic Acid
Sources: Sweetpotato Leaves, Propolis, Apples, White Grapes, White
Wine, Olives, Olive Oil, Spinach, Cabbage, Turnips, Radish,
Cauliflower, Bok Choy, Arugula, Kale, Asparagus, and Coffee.
en.wikipedia.org...
Caffeic Acid isn't related to Caffeine.
Growth Suppression of Human Cancer Cells by Polyphenolics from
Sweetpotato (Ipomoea batatas L.) Leaves
pubs.acs.org...
Sweetpotato leaves (Ipomoea batatas L.) contain a high content of
polyphenolics that consist of caffeic acid, chlorogenic acid,
3,4-di-O-caffeoylquinic acid, 3,5-di-O-caffeoylquinic acid,
4,5-di-O-caffeoylquinic acid, and 3,4,5-tri-O-caffeoylquinic acid. We
investigated the suppression of the proliferation of selected human
cancer cells by phenolic compounds isolated from sweetpotato leaf.
...Growth suppression of HL-60 cells by 3,4,5-tri-O-caffeoylquinic
acid was determined to be the result of apoptotic death of the cells.
These results indicate that 3,4,5-tri-O-caffeoylquinic acid may have
potential for cancer prevention.
Caffeic acid phenethyl ester induces mitochondria-mediated apoptosis
in human myeloid leukemia U937 cells
www.springerlink.com...
Caffeic acid phenyl ester (CAPE), a biologically active ingredient of
propolis, has several interesting biological properties including
antioxidant, anti-inflammatory, antiviral, immunostimulatory,
anti-angiogenic, anti-invasive, anti-metastatic and carcinostatic
activities. Recently, several groups have reported that CAPE is
cytotoxic to tumor cells but not to normal cells. In this study, we
investigated the mechanism of CAPE-induced apoptosis in human myeloid
leukemia U937 cells. Treatment of U937 cells with CAPE decreased cell
viability in a dose-dependent and time-dependent manner.
Caffeic Acid Phenethyl Ester Induces Apoptosis by Inhibition of NFκB
and Activation of Fas in Human Breast Cancer MCF-7 Cells
www.jbc.org...
Our findings demonstrate that NFκB inhibition is sufficient to induce
apoptosis and that Fas activation plays a role in NFκB
inhibition-induced apoptosis in MCF-7 cells.
The antioxidant caffeic acid phenethyl ester induces apoptosis
associated with selective scavenging of hydrogen peroxide in human
leukemic HL-60 cells
www.ncbi.nlm.nih.gov...
These results suggest that apoptosis induced by CAPE is associated
with mitochondrial dysfunction, GSH depletion and selective scavenging
of H2O2 in human leukemic HL-60 cells.
[edit on 22-8-2010 by IgnoranceIsntBlisss]
copyright & usage
reply posted on 22-8-2010 @ 03:12 PM by IgnoranceIsntBlisss
Effect of caffeic acid phenethyl ester on proliferation and apoptosis
of colorectal cancer cells in vitro
www.ncbi.nlm.nih.gov...
After HCT116 cells were exposed to CAPE (80, 40, 20, 10, 5, and 2.5
mg/L) for 24, 48, 72, 96 h, CAPE displayed a strong growth inhibitory
effect in a dose- and time-dependent manner against HCT116 cells. FCM
analysis showed that the ratio of G(0)/G(1) phase cells increased, S
phase ratio decreased and apoptosis rate increased after HCT116 cells
were exposed to CAPE (10, 5, and 2.5 mg/L) for 24 h. CAPE treatment
was associated with decreased cytoplasmic beta-catenin, nuclear
beta-catenin and a concurrent increase in beta-catenin protein
expression at cell-cell junctions.
Capsaicin
Foods: Hot Peppers.
Sources: Pepper Spray (It's probably a very bad idea to try and breath
this stuff).
Capsaicin (what makes peppers "hot") has been proven to trigger
apoptosis in multiple lines of cancer.
Capsaicin Displays Anti-Proliferative Activity against Human Small
Cell Lung Cancer in Cell Culture and Nude Mice Models via the E2F
Pathway
www.ncbi.nlm.nih.gov...
BrdU assays and PCNA ELISAs showed that capsaicin displays robust
anti-proliferative activity in four human SCLC cell lines.
Furthermore, capsaicin potently suppressed the growth of H69 human
SCLC tumors in vivo as ascertained by CAM assays and nude mice models.
The second part of our study attempted to provide insight into
molecular mechanisms underlying the anti-proliferative activity of
capsaicin. We found that the anti-proliferative activity of capsaicin
is correlated with a decrease in the expression of E2F-responsive
proliferative genes like cyclin E, thymidylate synthase, cdc25A and
cdc6, both at mRNA and protein levels.
Capsaicin-induced cell death in a human gastric adenocarcinoma cell line
www.wjgnet.com...
Capsaicin, a pungent ingredient found in red pepper, has long been
used in spices, food additives, and drugs. Cell death induced by the
binding of capsaicin was examined in a human gastric adenocarcinoma
cell line (AGS cells).
...Recently, a series of studies have demonstrated that capsaicin
inhibits mutagenicity and DNA binding of some chemical carcinogens,
possibly by suppressing their metabolic activation[16-18]. With cells
in culture, capsaicin-inhibited proliferation of HeLa, ovarian
carcinoma, and mammary adenocarcinoma by decreasing NADH oxidase
activity[19]. Capsaicin can also alter the expression of tumor
forming-related genes by mediating the overexpression of p53 and/or
c-myc genes in a Korean stomach cancer cell line[20]. Capsaicin was
found to induce apoptosis in T cells by increasing the reactive oxygen
species and by a subsequent mitochondrial ransmembrane potential[21].
In this report, we examined the underlying mechanism by which
capsaicin induces apoptotic cell death in a human gastric
adenocarcinoma cell line (AGS).
Capsaicin-induced apoptosis and reduced release of reactive oxygen
species in MBT-2 Murine Bladder Tumor cells
www.springerlink.com...
Capsaicin, the major pungent ingredient in genusCapsicum, has recently
been tried as an intravesical drug for overactive bladder and it has
also been shown to induce apoptotic cell death in many cancer cells.
In this study, we investigated the apoptosis-inducing effect and
alterations in the cellular redox state of capsaicin in MBT-2 murine
bladder tumor cells. Capsaicin induced apoptotic MBT-2 cell death in a
time- and dose-dependent manner. The capsaicin-induced apoptosis was
blocked by the pretreatment with Z-VAD-fmk, a broad-range caspase
inhibitor, or AcDEVD-CHO, a caspase-3 inhibitor.
Capsaicin-induced apoptosis in human breast cancer MCF-7 cells through
caspase-independent pathway
www.spandidos-publications.com...
Our results suggest that capsaicin induces cellular apoptosis through
a caspase-independent pathway in MCF-7 cells, and that reactive oxygen
species and intracellular calcium ion fluctuation has a minimal role
in the process.
TRPV6 mediates capsaicin-induced apoptosis in gastric cancer cells
www.ncbi.nlm.nih.gov...
In this study, both gastric cancer and normal epithelial cells were
treated with capsaicin and examined for apoptosis by Annexin V
binding. Our results showed that capsaicin induces apoptosis in both
cells, although cancer cells are more susceptible. This susceptibility
is dependent on the availability of TRPV6, a calcium-selective channel
protein, as overexpression of TRPV6 in normal cells increased
capsaicin-induced apoptosis and knockdown of TRPV6 in cancer cells
suppressed this action. Our results further demonstrated that
capsaicin increases mitochondrial permeability through activation of
Bax and p53 in a JNK-dependent manner.
Capsaicin Shows Promise In Inhibiting Growth Of Pancreatic Cancer
www.medicalnewstoday.com...
"In our study, we discovered that capsaicin fed orally to mice with
human pancreatic tumors was an extremely effective inhibitor of the
cancer process, inducing apoptosis in cancer cells," said Sanjay K.
Srivastava, Ph.D., lead investigator and assistant professor,
department of pharmacology, University of Pittsburgh School of
Medicine. "Capsaicin triggered the cancerous cells to die off and
significantly reduced the size of the tumors."
Capsaicin Mediates Cell Death in Bladder Cancer T24 Cells Through
Reactive Oxygen Species Production and Mitochondrial Depolarization
www.ncbi.nlm.nih.gov...
RESULTS: CAP decreased the viability of T24 cells in a dose-dependent
manner without marked apoptosis. CAP induced ROS production and
mitochondrial membrane depolarization, thereby inducing cell death,
not apoptosis, in T24 cells at a concentration of 100 microM or
higher. Furthermore, these effects of CAP could be reversed by
capsazepine, the antagonist of transient receptor potential vanilloid
type 1 channel. In vivo experiment showed that CAP significantly
slowed the growth of T24 bladder cancer xenografts as measured by size
(661.80 +/- 62.03 vs 567.02 +/- 43.94 mm(3); P <.01).
CONCLUSIONS: CAP mediates cell death in T24 cells through calcium
entry-dependent ROS production and mitochondrial depolarization, and
it may have a role in the management of bladder cancer.
Carotenoids
Foods: Carrots, Sweet Potato, Kale, Apricots, Mangos, Squash, Spinach,
Kale, Collard Greens, Salmon, Shellfish, Egg Yolks, Hot Peppers, Brown
Algae.
Carotenoids Affect Proliferation of Human Prostate Cancer Cells
jn.nutrition.org...
We investigated whether various carotenoids present in foodstuffs were
potentially involved in cancer-preventing action on human prostate
cancer. The effects of 15 kinds of carotenoids on the viability of
three lines of human prostate cancer cells, PC-3, DU 145 and LNCaP,
were evaluated. When the prostate cancer cells were cultured in a
carotenoid-supplemented medium for 72 h at 20 µmol/L, 5,6-monoepoxy
carotenoids, namely, neoxanthin from spinach and fucoxanthin from
brown algae, significantly reduced cell viability to 10.9 and 14.9%
for PC-3, 15.0 and 5.0% for DU 145, and nearly zero and 9.8% for
LNCaP, respectively.
Serum carotenoids and mortality from lung cancer
onlinelibrary.wiley.com...
Higher serum levels of carotenoids such as - and β-carotenes may play
a role in preventing death from lung cancer
Human Breast Cancer Cells Treated with Carotenoids or Retinoids
jn.nutrition.org...
These results demonstrate that ER status is an important, although not
essential factor for breast cancer cell response to carotenoid and
retinoid treatments, and the mode of action of all-t-RA in MCF-7 and
Hs578T cells is not through the induction of RAR. Other mechanistic
pathways that are either followed by or concomitant with growth
inhibition are possible.
Carotenoids, antioxidants and ovarian cancer risk in pre- and
postmenopausal women
onlinelibrary.wiley.com...
From a population-based study of 549 cases of ovarian cancer and 516
controls, we estimated the consumption of the antioxidant vitamins A,
C, D and E and various carotenoids, including alpha- and beta-carotene
and lycopene, using a validated dietary questionnaire. Multivariate
logistic regression was used to calculate the exposure odds ratios
adjusted for established ovarian cancer risk factors. Intakes of
carotene, especially alpha-carotene, from food and supplements were
significantly and inversely associated with risk for ovarian cancer,
predominantly in postmenopausal women. Intake of lycopene was
significantly and inversely associated with risk for ovarian cancer,
predominantly in premenopausal women. Food items most strongly related
to decreased risk for ovarian cancer were raw carrots and tomato
sauce. Consumption of fruits, vegetables and food items high in
carotene and lycopene may reduce the risk of ovarian cancer.
copyright & usage
reply posted on 22-8-2010 @ 03:15 PM by IgnoranceIsntBlisss
Ceramide
Source: Chemical supply houses.
www.scbt.com...
This one is interesting as it is synthesized in the body in response
to 'traditional' treatments. It seems obvious to go straight to it.
Ceramide mediates cancer therapy-induced apoptosis
www.ncbi.nlm.nih.gov...
Ceramide, which accumulates in response to different types of cellular
stress such as chemo- and radiotherapy, strongly induced expression of
CD95-L, cleavage of caspases and apoptosis. Antisense CD95-L as well
as dominant-negative FADD inhibited ceramide- and cellular
stress-induced apoptosis.
Induction of Apoptotic Cell Death and Prevention of Tumor Growth by Ceramide
cancerres.aacrjournals.org...
We measured the levels of ceramide, a candidate lipid mediator of
apoptosis, in human metastatic colorectal cancer and tested in vitro
and in vivo effects of various ceramide analogues in inducing
apoptosis in metastatic colon cancer. Human colon cancer showed a >50%
decrease in the cellular content of ceramide when compared with normal
colon mucosa.
Multidrug resistance modulators and doxorubicin synergize to elevate
ceramide levels and elicit apoptosis in drug-resistant cancer cells
www.ncbi.nlm.nih.gov...
These results demonstrate that MDR modulators can be used separately,
in combination, or in conjunction with chemotherapy at clinically
relevant concentrations to manipulate cellular ceramide levels and
restore sensitivity in the drug resistant setting. As such, this
represents a new direction in the treatment of cancer.
Ionizing radiation acts on cellular membranes to generate ceramide and
initiate apoptosis
www.ncbi.nlm.nih.gov...
The present studies show that ionizing radiation, like TNF, induces
rapid sphingomyelin hydrolysis to ceramide and apoptosis in bovine
aortic endothelial cells. Elevation of ceramide with exogenous
ceramide analogues was sufficient for induction of apoptosis. Protein
kinase C activation blocked both radiation-induced sphingomyelin
hydrolysis and apoptosis, and apoptosis was restored by ceramide
analogues added exogenously. Ionizing radiation acted directly on
membrane preparations devoid of nuclei, stimulating sphingomyelin
hydrolysis enzymatically through a neutral sphingomyelinase. These
studies provide the first conclusive evidence that apoptotic signaling
can be generated by interaction of ionizing radiation with cellular
membranes and suggest an alternative to the hypothesis that direct DNA
damage mediates radiation-induced cell kill.
Cinnamaldehyde
Food: Cinnamon
en.wikipedia.org...
Cinnamaldehyde induces apoptosis by ROS-mediated mitochondrial
permeability transition in human promyelocytic leukemia HL-60 cells
www.ncbi.nlm.nih.gov...
Cinnamaldehyde is an active compound isolated from the stem bark of
Cinnamomum cassia, a traditional oriental medicinal herb, which has
been shown to inhibit tumor cell proliferation. In this study, we
investigated the effects of cinnamaldehyde on the cytotoxicity,
induction of apoptosis and the putative pathways of its actions in
human promyelocytic leukemia cells. ...Taken together, our data
indicate that cinnamaldehyde induces the ROS-mediated mitochondrial
permeability transition and resultant cytochrome c release. This is
the first report on the mechanism of the anticancer effect of
cinnamaldehyde.
Induction of apoptotic cell death by 2′-hydroxycinnamaldehyde is
involved with ERK-dependent inactivation of NF-κB in TNF-α-treated
SW620 colon cancer cells
www.ncbi.nlm.nih.gov...
These results demonstrate that HCA inhibits cell growth through
induction of apoptotic cell death by ERK pathway-dependent NF-kappaB
inactivation.
More cinnamon, less cancer
www.torontosun.com...
It has been know for a few years that several types of spices contain
large amounts of cancer-fighting compounds that could help in the
prevention of the disease. In addition to the well-known health
properties of tumeric and ginger, a recent study has suggested that
cinnamon could be equally useful in reducing tumour growth by blocking
the formation of new vessels using a process called angiogenesis.
Cinnamon extract induces tumor cell death through inhibition of NFκB and AP1
www.biomedcentral.com...
Cinnamon extract strongly inhibited tumor cell proliferation in vitro
and induced active cell death of tumor cells by up-regulating
pro-apoptotic molecules while inhibiting NFκB and AP1 activity and
their target genes such as Bcl-2, BcL-xL and survivin. Oral
administration of cinnamon extract in melanoma transplantation model
significantly inhibited tumor growth with the same mechanism of action
observed in vitro.
Citral
Food: Lemon Grass
Sources: Asian grocery's (lemon grass), Health food stores (extracts).
An essential oil and its major constituent isointermedeol induce
apoptosis in human leukaemia HL-60 cells
www.ncbi.nlm.nih.gov...
An essential oil from a lemon grass variety of Cymbopogon flexuosus
(CFO) and its major chemical constituent sesquiterpene isointermedeol
(ISO) were investigated for their ability to induce apoptosis in human
leukaemia HL-60 cells because dysregulation of apoptosis is the
hallmark of cancer cells. ...The easy and abundant availability of the
oil combined with its suggested mechanism of cytotoxicity make CFO
highly useful in the development of anti-cancer therapeutics.
Citral is a New Inducer of Caspase-3 in Tumor Cell Lines
www.thieme-connect.com...
Citral, 3,7-dimethyl-2,6-octadien-1-al, a key component of the
lemon-scented essential oils extracted from several herbal plants such
as lemon grass (Cymbopogon citratus), melissa (Melissa officinalis),
verbena (Verbena officinalis) is used as a food additive and as a
fragrance in cosmetics. In this study, we investigated the anti-cancer
potential of citral and its mode of action. Concentrations of 44.5 μM,
comparable to the concentration of citral in a cup of tea prepared
from 1 g of lemon grass, induced apoptosis in several hematopoietic
cancer cell lines. Apoptosis was accompanied by DNA fragmentation and
caspase-3 catalytic activity induction. Citral activity (22.25 μM) was
compared to a reference compound like staurosporine (0.7 μM), in
respect to DNA fragmentation and caspase-3 enzymatic activity. The
apoptotic effect of citral depended on the α,β-unsaturated aldehyde
group.
Citral inhibits cell proliferation and induces apoptosis and cell
cycle arrest in MCF-7 cells
www.ncbi.nlm.nih.gov...
In this study, we investigated the effect of citral
(3,7-dimethyl-2,6-octadienal), a key component of essential oils
extracted from several herbal plants, on the proliferation rate, cell
cycle distribution, and apoptosis of the human breast cancer cell line
MCF-7. The effects of this compound were also tested on
cyclo-oxygenase activity. Citral treatment caused inhibition of MCF-7
cell growth (IC(50)-48 h: 18 x 10(-5)m), with a cycle arrest in G(2)/M
phase and apoptosis induction. Moreover, we observed a decrease in
prostaglandin E(2) synthesis 48 h after citral treatment. These
findings suggest that citral has a potential chemopreventive effect.
Cod Liver Oil
en.wikipedia.org...
Women and Lung Cancer - Could Cod Liver Oil Improve Survival
lungcancer.about.com...
My Scandinavian, cod-liver-oil-serving grandma was right again – based
on the results of a new Norwegian study. Women who used cod liver oil
daily for a year prior to their diagnosis of lung cancer, had a 44%
lower chance of dying. Though my grandmother would have turned 100
last week, support for her advice will be published next month in the
International Journal of Cancer. Researchers looked at questionnaires
completed by over 68,000 women between 1996 and 1999. They then
analyzed 2,242 women who developed cancer following the questionnaire
and up to the year 2007. Women who used cod liver oil daily, had a 23%
lower chance of dying from solid tumors in general (breast,
colorectal, and lung cancers), and a 44% reduced risk of dying from
lung cancer.
Coenzyme Q10
Foods: Fish, chicken, peanuts, seasame seeds, pistachios, olive oil,
soy beans, grapeseed, parsley, perilla, broccoli (and relatives).
Sources: Health food stores (extracts).
en.wikipedia.org...
Co-Q10 is present in most "eukaryotic" cells (muscle tissues and
more). It's produced naturally in the body, which uses it for cell
growth and to protect cells from damage that could lead to cancer. In
animals it's most concentrated in the heart. Co-Q10 both boosts the
immune system, and has been shown to induce apoptosis.
copyright & usage
reply posted on 22-8-2010 @ 03:16 PM by IgnoranceIsntBlisss
www.cancer.gov...
Low blood levels of coenzyme Q10 have been found in patients with
myeloma, lymphoma, and cancers of the breast, lung, prostate,
pancreas, colon, kidney, and head and neck. Studies suggest that
coenzyme Q10 may help the immune system work better. Partly because of
this, coenzyme Q10 is used as adjuvant therapy for cancer. Adjuvant
therapy is treatment given following the primary treatment to increase
the chances of a cure.
www.cancer.gov...
Clinical trials have shown that coenzyme Q10 helps protect the heart
from the damaging side effects of doxorubicin, a drug used to treat
cancer.
Normalizattion of BCL-2 family members in breast cancer by Coenzyme Q10
www.ishib.org...
Because of their integral role in intrinsic apoptosis any imbalance
can lead to a variety of diseases; under expression can lead to
degenerative diseases while over expression can lead to cancer and
autoimmune disease. Due to their life or death role in the cell, Bcl-2
family members are currently the targets of many therapies in various
disease states. Bcl-2 itself is over expressed in most tumors and all
anti-apoptotic Bcl-2 family members are considered to have oncogenic
potential. Conversely, the pro-apoptotic members are considered to be
tumor suppressors
and many mimetics are foci for cancer research. ...Both pro- and
anti-apoptotic protein levels were measured in the two breast cancer
cell lines after Q10 exposure. Protein levels were measured at 4,8,12,
and 24 hours respectively in order to capture evidence of Q10's
normalizing influence on disrupted apoptotic function. In the MCF-7
cell line Bcl-2 levels were seen to significantly drop after only 4
hours of Q10 exposure.
Copper (BAD)
Listing of foods that DO and DON'T contain copper:
www.gicare.com...
Substances that reduce copper include: Tetrathiomolybdate, Trientine,
Disulfiram, Penicillamine, Zinc and others. Look for entries for these
substances. Get a good water filter!
Role of copper in tumour angiogenesis--clinical implications
www.ncbi.nlm.nih.gov...
The formation of new blood vessels is the initial step in progressive
tumour development and metastasis. The first stage in tumour
angiogenesis is the activation of endothelial cells. Copper ions
stimulate proliferation and migration of endothelial cells. It has
been shown that serum copper concentration increases as the cancer
disease progresses and correlates with tumour incidence and burden.
Copper ions also activate several proangiogenic factors, e.g.,
vascular endothelial growth factor, basic fibroblast growth factor,
tumour necrosis factor alpha and interleukin 1. This review concerns a
brief introduction into the basics of tumour blood vessel development
as well as the regulatory mechanisms of this process. The role of
copper ions in tumour angiogenesis is discussed. The new
antiangiogenic therapies based on a reduction of copper levels in
tumour microenvironment are reviewed.
Increased Expression of the Copper Efflux Transporter ATP7A Mediates
Resistance to Cisplatin, Carboplatin, and Oxaliplatin in Ovarian
Cancer Cells
clincancerres.aacrjournals.org...
The 1.5-fold higher expression of ATP7A in the 2008/MNK cells was
sufficient to alter Cu cellular pharmacokinetics but not confer Cu
resistance. In contrast, it was sufficient to render the 2008/MNK
cells resistant to cisplatin, carboplatin, and oxaliplatin. Resistance
was associated with increased rather than decreased whole-cell Pt drug
accumulation and increased sequestration of Pt into the vesicular
fraction. Cu triggered relocalization of ATP7A away from the
perinuclear region, whereas at equitoxic concentrations the Pt drugs
did not.
Cuminum Cyminum
Food: Cumin Seeds.
en.wikipedia.org...
Primary ingredient in Chili Powder.
Cumin: natures potent cancer combatant
findarticles.com...
This herb has been seen to effectively decrease the incidence of
chemically induced tumors of the stomach, colon, and cervix. Its
significant antioxidant activity and the ability to modulate the
metabolism of carcinogens (toxins) explain its cancer-preventive
prowess. Cumin seeds are known to induce the activity of
glutathione-S-transferase, a protective enzyme that helps eliminate
cancer-causing substances. Cumin offers a significant level of
caffeic, chlorogenic, ferulic, and other phenolic acids that have
anti-inflammatory potential.
Antitumor and Antibacterial Activities of ...Cuminum Cyminum Seeds
www.insipub.com...
1-(2-Ethyl, 6-Heptyl) Phenol (EHP), a biologically active compound
formerly extracted bybenzene from Cuminum cyminum (cumin) Egyptian
seeds and of activity against a number of fungalpathogens, exhibited
antitumor activity against six types of tumor cell lines (HEPG2, HELA,
HCT116,MCF7, HEP2, CACO2).
Curcumin
Foods: Tumeric roots / powder, curry powder, yellow mustard.
Sources: Health food stores (extracts), large farmers markets (roots),
Indian grocery stores (tumeric powder in bulk).
en.wikipedia.org...
Tumeric has been proven to kill throat cancer cells. It seems obvious
that the effectiveness in the case of throat cancer is from the
curcumin, the active ingredient, passing directly over the cancer
cells. Therefore, the I.I.B. idea for lung cancer is to run liquid
curcumin extract thru a "nebulizer" apparatus to inhale it. Check back
for updates as to whether or not this turns out to be harsh on the
lungs.
Turmeric Spice Kills Throat Cancer Cells
www.associatedcontent.com...
news.bbc.co.uk...
On Tuesday, the British Journal of Cancer published a propitious study
from Cork Cancer Research Centre ("CCRC") at the University College
Cork in Ireland that found that curcumin—a compound in the curry spice
turmeric—begins killing esophageal cancer cells within 24 hours.
According to the CCRC study, curcumin ostensibly acts as a free
radical scavenger that triggers a lethal cell death signal that causes
cancerous cells in the throat to digest and kill themselves.
Induction of apoptosis in human lung cancer cells by curcumin
www.cancerletters.info...(04)00053-9/abstract
This study investigated the cellular and molecular changes induced by
curcumin leading to the induction of apoptosis in human lung cancer
cell lines—A549 and H1299. A549 is p53 proficient and H1299 is p53
null mutant. The lung cancer cells were treated with curcumin (0–160
μM) for 12–72 h. Curcumin inhibited the growth of both the cell lines
in a concentration dependent manner. Growth inhibition of H1299 cell
lines was both time and concentration dependent. Curcumin induced
apoptosis in both the lung cancer cell lines. A decrease in expression
of p53, bcl-2, and bcl-XL was observed after 12 h exposure of 40 μM
curcumin. Bak and Caspase genes remained unchanged up to 60 μM
curcumin but showed decrease in expression levels at 80–160 μM. The
data also suggest a p53 independent induction of apoptosis in lung
cancer cells.
Curcumin induces apoptosis in immortalized NIH 3T3 and malignant
cancer cell lines
www.ncbi.nlm.nih.gov...
Curcumin, which is a widely used dietary pigment and spice, has been
demonstrated to be an effective inhibitor of tumor promotion in mouse
skin carcinogenesis. We report that curcumin induces cell shrinkage,
chromatin condensation, and DNA fragmentation, characteristics of
apoptosis, in immortalized mouse embryo fibroblast NIH 3T3 erb B2
oncogene-transformed NIH 3T3, mouse sarcoma S180, human colon cancer
cell HT-29, human kidney cancer cell 293, and human hepatocellular
carcinoma Hep G2 cells
Curcumin induces apoptosis in human breast cancer cells
linkinghub.elsevier.com...
The aim of this study was to determine the mechanisms of
curcumin-induced human breast cancer cell apoptosis. From quantitative
image analysis data showing an increase in the percentage of cells
with a sub-G0/G1 DNA content, we demonstrated curcumin-induced
apoptosis in the breast cancer cell line MCF-7, in which expression of
wild-type p53 could be induced. Apoptosis was accompanied by an
increase in p53 level as well as its DNA-binding activity followed by
Bax expression at the protein level. Further experiments using
p53-null MDAH041 cell as well as low and high p53-expressing TR9-7
cell, in which p53 expression is under tight control of tetracycline,
established that curcumin induced apoptosis in tumor cells via a
p53-dependent pathway in which Bax is the downstream effector of p53.
This property of curcumin suggests that this molecule could have a
possible therapeutic potential in breast cancer patients.
[edit on 22-8-2010 by IgnoranceIsntBlisss]
copyright & usage
reply posted on 22-8-2010 @ 03:19 PM by IgnoranceIsntBlisss
Curcumin inhibits proliferation, induces apoptosis, and inhibits
angiogenesis of LNCaP prostate cancer cells in vivo
onlinelibrary.wiley.com...
Curcumin causes a marked decrease in the extent of cell proliferation
as measured by the BrdU incorporation assay and a significant increase
in the extent of apoptosis as measured by an in situ cell death assay.
Moreover, a significant decrease in the microvessel density as
measured by the CD31 antigen staining was also seen.
Chemopreventive Effect of Curcumin...during the Promotion/Progression
Stages of Colon Cancer
cancerres.aacrjournals.org...
The inhibition of adenocarcinomas of the colon was, in fact, dose
dependent. Administration of curcumin to the rats during the
initiation and postinitiation stages and throughout the
promotion/progression stage increased apoptosis in the colon tumors as
compared to colon tumors in the groups receiving AOM and the control
diet. Thus, chemopreventive activity of curcumin is observed when it
is administered prior to, during, and after carcinogen treatment as
well as when it is given only during the promotion/progression phase
(starting late in premalignant stage) of colon carcinogenesis.
Notch-1 down-regulation by curcumin is associated with the inhibition
of cell growth and the induction of apoptosis in pancreatic cancer
cells
onlinelibrary.wiley.com...
Curcumin inhibited cell growth and induced apoptosis in pancreatic
cancer cells. Notch-1, Hes-1, and Bcl-XL expression levels
concomitantly were down-regulated by curcumin treatment. These results
correlated with the inactivation of NF-κB activity and increased
apoptosis induced by curcumin. The down-regulation of Notch-1 by
small-interfering RNA prior to curcumin treatment resulted in enhanced
cell growth inhibition and apoptosis.
Curcumin, an antioxidant and anti-tumor promoter, induces apoptosis in
human leukemia cells
www.ncbi.nlm.nih.gov...
Curcumin, widely used as a spice and coloring agent in food, possesses
potent antioxidant, anti-inflammatory and anti-tumor promoting
activities. In the present study, curcumin was found to induce
apoptotic cell death in promyelocytic leukemia HL-60 cells at
concentrations as low as 3.5 micrograms/ml.
Antiproliferation and apoptosis induced by curcumin in human ovarian
cancer cells
www.ncbi.nlm.nih.gov...
Curcumin, an active ingredient from the rhizome of the plant, Curcuma
longa, has antioxidant, anti-inflammatory and anti-cancer activities.
It has recently been demonstrated that the chemopreventive activities
of curcumin might be due to its ability to inhibit cell growth and
induce apoptosis. In the present study, we have investigated the
effects of curcumin on growth and apoptosis in the human ovarian
cancer cell line Ho-8910 by MTT assay, fluorescence microscopy, flow
cytometry and Western blotting. Our data revealed that curcumin could
significantly inhibit the growth and induce apoptosis in Ho-8910
cells. A decrease in expression of Bcl-2, Bcl-X(L) and pro-caspase-3
was observed after exposure to 40 microM curcumin, while the levels of
p53 and Bax were increased in the curcumin-treated cells. These
activities may contribute to the anticarcinogenic action of curcumin.
Daidzein
Foods: Soybeans, Kwao Krua & Kudzu.
en.wikipedia.org...
Biphasic effect of daidzein on cell growth of human colon cancer cells
www.ncbi.nlm.nih.gov...
LoVo cells were treated with 0.1, 1, 5, 10, 50 and 100 microM daidzein
for 2, 3, 4 or 5 d. The results indicated that daidzein stimulated the
growth of LoVo cells at 0.1 and 1 microM whereas at higher
concentrations (10, 50 and 100 microM) cell growth was inhibited in a
dose-dependent manner. Treatment of daidzein at 10, 50 and 100 microM
resulted in cell cycle arrest at G0/G1 phase, DNA fragmentation and
increases in caspase-3 activity. There were no changes in alkaline
phosphatase activity (ALP), an indicator of cell differentiation, upon
treatment with daidzein when compared to controls. These results
indicate that daidzein has a biphasic effect on LoVo cell growth and
its tumor suppressive effect is by means of cell cycle arrest and
apoptosis but not through cell differentiation.
Effect of daidzein on cell growth, cell cycle, and telomerase activity
of human cervical cancer in vitro
onlinelibrary.wiley.com...
The inductive effects of apoptosis were more obviously observed in
low-concentration groups. After HeLa cells were treated with daidzein,
the expression of human telomerase catalytic subunit mRNA decreased.
These meant that daidzein affected human nonhormone-dependent cervical
cancer cells in several ways, including cell growth, cell cycle, and
telomerase activity in vitro.
Effects of daidzein on estrogen-receptor-positive and negative
pancreatic cancer cells in vitro
www.ncbi.nlm.nih.gov...
Daidzein has antiproliferative effects on human
estrogen-receptor-positive and negative pancreatic cancer cells, but
their mechanisms may be different.
YouTube Link
Dichloroacetic Acid (DCA)
Sources: Chemical & pharmaceutical supply companies, Internet, doctors
prescription (if they're willing).
When I began this study this was at the top of my list of 'suppressed'
substances that I knew of. It made national news a few years ago when
the study was published. The big story seemed to be that it wasn't
patentable so therefore it wasn't going to go through extensive human
trails because it wasn't going to make anybody rich. While that is a
big story, now that I've completed this study I'm revising this entry.
The real big story is that there are seemingly endless compounds and
substances that are well studied and published that do the same thing,
and almost none of them are aggressively pursued by the medical
industry. Small teams of curious researchers study new ways of killing
cancer with all sorts of things, but unless there is a way for Big
Pharm to make endless billions then the medical community basically
does nothing with it. I know this first hand now that my mother is
going through this process and her doctors haven't told her to eat or
take anything that doesn't come from Big Pharm, and they cringe and
squirm when she tries to inquire about any of these known cancer
killers.
As it turns out, it costs in the range of hundreds of millions of
dollars to complete human trials for FDA approval of substances and
treatments, and there is quite literally no place in the FDA approval
process for anything that cannot be patented. The case of DCA has
helped underscore the need for something on the order of a 'Public
Domain Drug Act', where the public has weight in the approval process
of safe substances that show promise.
www.thedcasite.com...
You can get DCA if you dig around online. I found one site in the EU
where DCA costs about $30 for about 10,000 doses.
The following site has lots of useful information including treatment
testimonials:
www.thedcasite.com...
Some tidbits from my research:
Do not add DCA to hot or warm beverages. DCA is unstable at higher
temperatures. DCA can interact favorably or negatively with
chemotherapy is some patients. This is hard to predict unless a
chemosensitivity test like ChemoFit is performed.
www.youtube.com...
The Official University of Alberta DCA Website
www.dca.med.ualberta.ca...
DCA is an odourless, colourless, inexpensive, relatively non-toxic,
small molecule. And researchers at the University of Alberta believe
it may soon be used as an effective treatment for many forms of
cancer. Dr. Evangelos Michelakis, a professor at the U of A Department
of Medicine, has shown that dichloroacetate (DCA) causes regression in
several cancers, including lung, breast, and brain tumors.
A Mitochondria-K+ Channel Axis Is Suppressed in Cancer and Its
Normalization Promotes Apoptosis and Inhibits Cancer Growth
www.cell.com...
The unique metabolic profile of cancer (aerobic glycolysis) might
confer apoptosis resistance and be therapeutically targeted. Compared
to normal cells, several human cancers have high mitochondrial
membrane potential (m) and low expression of the K+ channel Kv1.5,
both contributing to apoptosis resistance. Dichloroacetate (DCA)
inhibits mitochondrial pyruvate dehydrogenase kinase (PDK), shifts
metabolism from glycolysis to glucose oxidation, decreases m,
increases mitochondrial H2O2, and activates Kv channels in all cancer,
but not normal, cells; DCA upregulates Kv1.5 by an NFAT1-dependent
mechanism. DCA induces apoptosis, decreases proliferation, and
inhibits tumor growth, without apparent toxicity. Molecular inhibition
of PDK2 by siRNA mimics DCA. The mitochondria-NFAT-Kv axis and PDK are
important therapeutic targets in cancer; the orally available DCA is a
promising selective anticancer agent.
[edit on 22-8-2010 by IgnoranceIsntBlisss]
copyright & usage
reply posted on 22-8-2010 @ 03:22 PM by IgnoranceIsntBlisss
DCA Research Team publishes results of Clinical Trials
www.dca.med.ualberta.ca...
In 2007 the U of A team led by Dr Michelakis, published evidence that
DCA reverses cancer growth in non-human models and test tubes. The
team showed then that DCA achieves these antitumor effects by altering
the metabolism of cancer. By altering the way cancer handles its
nutrient fuels, specifically the sugars, DCA was able to take away
cancer's most important strength, the resistance to death. Since then,
several independent groups across the world have confirmed the Alberta
team's findings. In December 2009, the editors of "Science" predicted
that cancer metabolism is one of only 5 areas across all scientific
disciplines, to "watch for major breakthroughs" in 2010.
Other smaller studies are being performed around the wrold. The
following site is another excellent source of data on real life human
trials:
www.medicorcancer.com...
Disulfiram
Removes copper from your system. This one should be good for
alcoholics diagnosed with cancer.
Disulfiram, a Clinically Used Anti-Alcoholism Drug and Copper-Binding
Agent, Induces Apoptotic Cell Death in Breast Cancer
cancerres.aacrjournals.org...
Copper has been shown to be essential for tumor angiogenesis
processes. Consistently, high serum and tissue levels of copper have
been found in many types of human cancers, including breast, prostate,
and brain, supporting the idea that copper could be used as a
potential tumor-specific target. Here we report that the DSF-copper
complex potently inhibits the proteasomal activity in cultured breast
cancer MDA-MB-231 and MCF10DCIS.com cells, but not normal,
immortalized MCF-10A cells, before induction of apoptotic cancer cell
death. Furthermore, MDA-MB-231 cells that contain copper at
concentrations similar to those found in patients, when treated with
just DSF, undergo proteasome inhibition and apoptosis. In addition,
when administered to mice bearing MDA-MB-231 tumor xenografts, DSF
significantly inhibited the tumor growth (by 74%), associated with in
vivo proteasome inhibition (as measured by decreased levels of tumor
tissue proteasome activity and accumulation of ubiquitinated proteins
and natural proteasome substrates p27 and Bax) and apoptosis induction
(as shown by caspase activation and apoptotic nuclei formation).
Electricity
Nanosecond pulsed electric fields induce apoptosis in p53-wildtype and
p53-null HCT116 colon carcinoma cells
www.springerlink.com...
Non-ionizing radiation produced by nanosecond pulsed electric fields
(nsPEFs) is an alternative to ionizing radiation for cancer treatment.
NsPEFs are high power, low energy (non-thermal) pulses that, unlike
plasma membrane electroporation, modulate intracellular structures and
functions. To determine functions for p53 in nsPEF-induced apoptosis,
HCT116p53+/+ and HCT116p53−/− colon carcinoma cells were exposed to
multiple pulses of 60 kV/cm with either 60 ns or 300 ns durations and
analyzed for apoptotic markers. Several apoptosis markers were
observed including cell shrinkage and increased percentages of cells
positive for cytochrome c, active caspases, fragmented DNA, and Bax,
but not Bcl-2. Unlike nsPEF-induced apoptosis in Jurkat cells (Beebe
et al. 2003a) active caspases were observed before increases in
cytochrome c, which occurred in the presence and absence of Bax. Cell
shrinkage occurred only in cells with increased levels of Bax or
cytochrome c. NsPEFs induced apoptosis equally in HCT116p53+/+ and
HCT116p53−/− cells. These results demonstrate that non-ionizing
radiation produced by nsPEFs can act as a non-ligand agonist with
therapeutic potential to induce apoptosis utilizing
mitochondrial-independent mechanisms in HCT116 cells that lead to
caspase activation and cell death in the presence or absence of p-53
and Bax.
Ellagic Acid
Foods: Blackberries, Raspberries, Strawberries, Cranberries, Grapes,
Walnuts, Pecans, Pomegranates, Wolfberry (Goji Berry) and numerous
other fruits and vegetables.
Ellagic acid induces apoptosis through inhibition of nuclear factor
kappa B in pancreatic cancer cells
www.ncbi.nlm.nih.gov...
We show that ellagic acid, a polyphenolic compound in fruits and
berries, at concentrations 10 to 50 mmol/L stimulates apoptosis in
human pancreatic adenocarcinoma cells. Further, ellagic acid decreases
proliferation by up to 20-fold at 50 mmol/L. Ellagic acid stimulates
the mitochondrial pathway of apoptosis associated with mitochondrial
depolarization, cytochrome C release, and the downstream caspase
activation. Ellagic acid does not directly affect mitochondria.
Ellagic acid dose-dependently decreased NF-kappa B binding activity.
Furthermore, inhibition of NF-kappa B activity using IkB wild type
plasmid prevented the effect of ellagic acid on apoptosis.
p53/p21(WAF1/CIP1) expression and its possible role in G1 arrest and
apoptosis in ellagic acid treated cancer cells
www.cancerletters.info...(98)00323-1/abstract
Ellagic acid is a phenolic compound present in fruits and nuts
including raspberries, strawberries and walnuts. It is known to
inhibit certain carcinogen-induced cancers and may have other
chemopreventive properties. The effects of ellagic acid on cell cycle
events and apoptosis were studied in cervical carcinoma (CaSki) cells.
We found that ellagic acid at a concentration of 10−5 M induced G1
arrest within 48 h, inhibited overall cell growth and induced
apoptosis in CaSki cells after 72 h of treatment. Activation of the
cdk inhibitory protein p21 by ellagic acid suggests a role for ellagic
acid in cell cycle regulation of cancer cells.
Ellagic Acid Induced p53/p21 Expression, G1 Arrest and Apoptosis in
Human Bladder Cancer T24 Cells
ar.iiarjournals.org...
Ellagic acid significantly reduced the viable cells, induced
G0/G1-phase arrest of the cell cycle and apoptosis. Ellagic acid also
increased p53 and p21 and decreased CDK2 gene expression, that may
lead to the G0/G1 arrest of T24 cells. Ellagic acid also promoted
caspase-3 activity after exposure for 1, 3, 6, 12 and 24 h, which led
to induction of apoptosis. Furthermore, the ellagic acid-induced
apoptosis on T24 cells was blocked by the broad-spectrum caspase
inhibitor (z-VAD-fmk).
Low Concentrations of Quercetin and Ellagic Acid Synergistically
Influence Proliferation, Cytotoxicity and Apoptosis in MOLT-4 Human
Leukemia Cells
jn.nutrition.org...
Ellagic acid significantly potentiated the effects of quercetin (at 5
and 10 µmol/L each) in the reduction of proliferation and viability
and the induction of apoptosis. Significant alterations in cell cycle
kinetics were also observed. The synergy was confirmed by an
isobolographic analysis of the cell proliferation data. The
interaction of ellagic acid and quercetin demonstrated an enhanced
anticarcinogenic potential of polyphenol combinations, which was not
based solely on the additive effect of individual compounds, but
rather on synergistic biochemical interactions.
Emodin
Source: Rheum Emodi (a Himalayan rhubarb).
en.wikipedia.org...
Emodin induces apoptosis of human cervical cancer cells
www.ncbi.nlm.nih.gov...
Emodin (1,3,8-trihydroxy-6-methylanthraquinone) is an active herbal
component traditionally used in China for treating various ailments.
Emodin exerts antiproliferative effects in many cancer cell lines and
the actual molecular mechanism of which is still not clear. Since
apoptosis could be a potential mechanism to explain these effects, we
tested whether emodin induces cell death in human cervical cancer
cells. Our results suggest that emodin exerts antiproliferative
effects in human cervical cancer cells. Emodin inhibited DNA synthesis
and induced apoptosis as demonstrated by increased nuclear
condensation, annexin binding and DNA fragmentation in Bu 25TK cells
in the presence of emodin. Moreover, we demonstrate for the first time
in human cervical cancer cells that the apoptotic pathway involved in
emodin-induced apoptosis is caspase-dependent and presumably through
the mitochondrial pathway, as shown by the activation of caspases-3,
-9 and cleavage of poly(ADP-ribose) polymerase.
Epigallocatechin
Foods: Green Tea (not Black Tea).
en.wikipedia.org...
copyright & usage
AboveTopSecret.com is advertising supported.
reply posted on 22-8-2010 @ 03:23 PM by IgnoranceIsntBlisss
Role of epigallocatechin gallate (EGCG) in the treatment of breast and
prostate cancer
www.ncbi.nlm.nih.gov...
Green tea and its major constituent epigallocatechin gallate (EGCG)
have been extensively studied as a potential treatment for a variety
of diseases, including cancer. Epidemiological data have suggested
that EGCG may provide protective effects against hormone related
cancers, namely breast or prostate cancer. Extensive in vitro
investigations using both hormone responsive and non-responsive cell
lines have shown that EGCG induces apoptosis and alters the expression
of cell cycle regulatory proteins that are critical for cell survival
and apoptosis. This review will highlight the important in vitro
mechanistic actions elicited by EGCG in various breast and prostate
cancer cell lines. Additionally, the actions of green tea/EGCG in in
vivo models for these cancers as well as in clinical trials will be
discussed.
Epigallocatechin-3-gallate induces mitochondrial membrane
depolarization and caspase-dependent apoptosis in pancreatic cancer
cells
carcin.oxfordjournals.org...
In pursuit of our investigations to dissect the molecular mechanism of
EGCG action on pancreatic cancer, we observed that the
antiproliferative action of EGCG on pancreatic carcinoma is mediated
through programmed cell death or apoptosis as evident from nuclear
condensation, caspase-3 activation and poly-ADP ribose polymerase
(PARP) cleavage. EGCG-induced apoptosis of pancreatic cancer cells is
accompanied by growth arrest at an earlier phase of the cell cycle.
Topical applications of caffeine or (−)-epigallocatechin gallate
(EGCG) inhibit carcinogenesis and selectively increase apoptosis in
UVB-induced skin tumors in mice
www.pnas.org...
SKH-1 hairless mice were irradiated with ultraviolet B (UVB) twice
weekly for 20 weeks. These tumor-free mice, which had a high risk of
developing skin tumors during the next several months, were then
treated topically with caffeine (6.2 μmol) or (−)-epigallocatechin
gallate (EGCG; 6.5 μmol) once a day 5 days a week for 18 weeks in the
absence of further treatment with UVB. Topical applications of
caffeine to these mice decreased the number of nonmalignant and
malignant skin tumors per mouse by 44% and 72%, respectively. Topical
applications of EGCG decreased the number of nonmalignant and
malignant tumors per mouse by 55% and 66%, respectively.
Immunohistochemical analysis showed that topical applications of
caffeine or EGCG increased apoptosis as measured by the number of
caspase 3-positive cells in nonmalignant skin tumors by 87% or 72%,
respectively, and in squamous cell carcinomas by 92% or 56%,
respectively, but there was no effect on apoptosis in nontumor areas
of the epidermis.
A component of green tea, (-)-epigallocatechin-3-gallate, promotes
apoptosis in T24 human bladder cancer cells
www.ncbi.nlm.nih.gov...
Bladder cancer is the fourth most common cancer in men and ninth most
common in women. It has a protracted course of progression and is thus
an ideal candidate for chemoprevention strategies and trials. This
study was conducted to evaluate the chemopreventive/antiproliferative
potential of (-)-epigallocatechin gallate (EGCG, the major
phytochemical in green tea) against bladder cancer and its mechanism
of action. Using the T24 human bladder cancer cell line, we found that
EGCG treatment caused dose- and time-dependent inhibition of cellular
proliferation and cell viability, and induced apoptosis.
Mechanistically, EGCG inhibits phosphatidylinositol 3'-kinase/Akt
activation that, in turn, results in modulation of Bcl-2 family
proteins, leading to enhanced apoptosis of T24 cells. These findings
suggest that EGCG may be an important chemoprevention agent for the
management of bladder cancer.
Erythropoietin (BAD)
en.wikipedia.org...
At first I had misread an abstract headline and thought that "EPO" was
another thing that fights cancer. So I went looking for substances
that boost it, and found that Echinacea (ECH) does the job. Then I
looked up Echinacea for fighting cancer and found several abstracts
stating such. Next I went back to EPO to pull up all of its abstracts
and realized that it's shown to help hypoxic tumor cells (tumors low
on oxygen) resist apoptosis. Therefore, ECH is also bad for fighting
hypoxic tumor cells. From there I found that cancer treatments often
cause anemia, and anti-anemia drugs actually help boost EPO. These
drugs (a multi-billion dollar a year micro-industry) are often given
with chemotherapy, and despite the scientific community realizing
these effects the FDA voted to still allow this methodology. There are
still several studies showing usefulness with ECH, but unless you know
detailed specifics about your particular cancer there are too many
alternatives to even consider it.
The effect of 4 wk of oral echinacea supplementation on serum
erythropoietin and indices of erythropoietic status
www.ncbi.nlm.nih.gov...
These data indicate that ECH supplementation resulted in an increase
in EPO and IL-3 but did not significantly alter RBCs, Hb, or Hct.
Erythropoietin signaling inhibits hypoxia-induced apoptosis in human
breast ecarcinoma cells
www.ncbi.nlm.nih.gov...
In the current study we provide evidence that increased autocrine Epo
signaling induced by moderate levels of hypoxia inhibits
hypoxia-induced apoptosis and promotes survival in MCF-7 human breast
cancer cells. The anti-apoptotic effect of Epo correlates with
upregulation of bcl-2 and bcl-XL, suggesting a mechanism similar to
those described in hematopoietic cells. The resulting decreased
apoptotic potential of hypoxic tumor cells may contribute to increased
aggressiveness and therapy resistance of breast cancers.
Government advisors support keeping anti-anemia drugs from Amgen and
Johnson & Johnson on the market for chemo patients
money.cnn.com...
The advisors voted 13-1 to keep Amgen's Aranesp and J&J's Procrit on
the market for use with chemotherapy, said Amgen. The drugs are used
to keep blood cell count from dropping and are often used with chemo,
which can cause anemia in patients. It was welcome news for both
companies, and both stocks closed up higher in Thursday trading.
Billions of dollars in annual sales stem from the use of these drugs
in chemo patients.
Ethylene Vinyl Acetate (BAD)
Source: Fire Safe Cigarettes
en.wikipedia.org...
This is the oil derived polymer that makes the new cigarettes "fire
safe". It's now mandatory in almost every state. Obviously cigarettes
are a strong cause of several forms of cancer, and that's the point:
why are they adding this chemical into them which promise to trigger a
mass scale cancer epidemic? If you can't quit smoking do whatever you
can to get off of this form of cigarettes.
Results of a Long-term Experimental Study on the Carcinogenicity of
Vinyl Acetate Monomer in Mice
www.ncbi.nlm.nih.gov...
Vinyl acetate monomer (VAM) was administered in drinking water at
doses of 5,000, 1,000, and 0 ppm (v/v), to Swiss mice, 17 weeks old
(breeders) or 12-day embryos (offspring) at the start of the
experiment. The treatment lasted 78 weeks, and the animals were kept
under control until spontaneous death. VAM has been shown to cause an
increase in: (1) total malignant tumors; (2) carcinomas of the Zymbal
glands, oral cavity, tongue, esophagus, and forestomach; (3) stomach
tumors; (4) lung tumors; and (5) uterine tumors. A slight increase of
hepatomas has been observed among male mice offspring treated with the
higher dose. On the basis of these data VAM must be considered a
multipotential carcinogen.
Evening Primrose
en.wikipedia.org...
Plant oil acts like cancer drug
news.bbc.co.uk...
Scientists have pinpointed how evening primrose oil fights breast
tumours. It is down to a substance in the oil called gamma-linolenic
acid that acts on the same receptor in tumours as the powerful breast
cancer drug Herceptin. Unlike Herceptin, which blocks the Her-2/neu
receptor, GLA interferes with the gene carrying the DNA code needed to
make the receptor work. The US work in the Journal of the National
Cancer Institute applies to about 30% breast cancers.
Caspase-independent apoptosis induced by evening primrose extract in
Ehrlich ascites tumor cells
www.ncbi.nlm.nih.gov...
The EPE-induced translocation of AIF was suppressed with the addition
of catalase, suggesting that the rapid intracellular peroxide levels
after addition of EPE triggers off induction of apoptosis, which is
AIF-mediated and caspase-independent.
Figs
en.wikipedia.org...
Figs seem to have usefulness in fighting cancer, and also help the appetite.
[edit on 22-8-2010 by IgnoranceIsntBlisss]
copyright & usage
reply posted on 22-8-2010 @ 03:24 PM by IgnoranceIsntBlisss
Suppressors of Cancer Cell Proliferation from Fig (Ficus carica) Resin
pubs.acs.org...
A mixture of 6-O-acyl-β-d-glucosyl-β-sitosterols, the acyl moeity
being primarily palmitoyl and linoleyl with minor amounts of stearyl
and oleyl, has been isolated as a potent cytotoxic agent from fig
(Ficus carica) latex and soybeans. Identity was established by
spectroscopic methods (NMR, MS) and confirmed by chemical synthesis.
Both the natural and the synthetic compounds showed in vitro
inhibitory effects on proliferation of various cancer cell lines.
Fisetin
en.wikipedia.org...
Fisetin can be found in various plants such as Acacia greggii, Acacia
berlandieri, in the yellow dye young fustic from Rhus cotinus
(Eurasian smoketree), in Butea frondosa (parrot tree), Gleditschia
triacanthos, Quebracho colorado and the genus Rhus and in Callitropsis
nootkatensis (yellow cypresses). It is also reported in mangoes.
Fisetin, a novel dietary flavonoid, causes apoptosis and cell cycle
arrest in human prostate cancer LNCaP cells
carcin.oxfordjournals.org...
There was also induction of mitochondrial release of cytochrome c into
cytosol, downregulation of X-linked inhibitor of apoptosis protein and
upregulation of second mitochondria-derived activator of
caspase/direct inhibitor of apoptosis-binding protein with low pI on
treatment of cells with fisetin. Treatment of cells with fisetin also
resulted in significant activation of caspases-3, -8 and -9.
Pretreatment of cells with caspase inhibitor (Z-VAD-FMK) blocked
fisetin-induced activation of caspases. These data provide the first
evidence that fisetin could be developed as an agent against PCa.
A plant flavonoid fisetin induces apoptosis in colon cancer cells by
inhibition of COX2 and Wnt/EGFR/NF-B-signaling pathways
carcin.oxfordjournals.org...
Fisetin treatment of cells also inhibited the activation of EGFR and
nuclear factor-kappa B (NF-B). Finally, the formation of colonies in
soft agar was suppressed by fisetin treatment. Taken together, we
provide evidence that the plant flavonoid fisetin can induce apoptosis
and suppress the growth of colon cancer cells by inhibition of COX2-
and Wnt/EGFR/NF-B-signaling pathways. We suggest that fisetin could be
a useful agent for prevention and treatment of colon cancer.
Flavonoids Induce Apoptosis in Human Leukemia U937 Cells Through
Caspase- and Caspase-Calpain-Dependent Pathways
www.ncbi.nlm.nih.gov...
At lower concentrations, these compounds were also able to sensitize
these cells to apoptosis induced by tumor necrosis factor-. Regarding
the mechanisms, galangin, luteolin, chrysin, and quercetin induced
apoptosis in a way that required the activation of caspases 3 and 8,
but not caspase 9. In contrast, an active role of calpains in addition
to caspases was demonstrated in apoptosis induced by fisetin,
apigenin, and 3,7-dihydroxyflavone. Our data show evidence of the
proapoptotic properties of some flavonoids that could support their
rational use as chemopreventive and therapeutic agents against
carcinogenic disease.
Fisetin Inhibits Androgen Receptor Signaling and Tumor Growth in
Athymic Nude Mice
cancerres.aacrjournals.org...
Treatment with fisetin in athymic nude mice implanted with AR-positive
CWR22Rυ1 human PCa cells resulted in inhibition of tumor growth and
reduction in serum PSA levels. These data identify fisetin as an
inhibitor of AR signaling axis and suggest that it could be a useful
chemopreventive and chemotherapeutic agent to delay progression of
PCa.
Fucoidan
Foods: Various species of brown seaweed such as Kombu, Limu Moui,
Bladderwrack, Wakame, Mozuku, and Hijiki.
Sources: Extracts under various names including "Modifilan".
Apoptosis inducing activity of fucoidan in HCT-15 colon carcinoma cells
www.ncbi.nlm.nih.gov...
The antitumor activity of fucoidan from Fucus vesiculosus was
investigated in human colon carcinoma cells. The crude fucoidan, a
polysaccharide composed predominantly of sulfated fucose, markedly
inhibited the growth of HCT-15 cells (human colon carcinoma cells).
After HCT-15 cells were treated with fucoidan, several apoptotic
events such as DNA fragmentation, chromatin condensation and increase
of the population of sub-G1 hypodiploid cells were observed.
...Furthermore, the induction of apoptosis was also accompanied by a
strong activation of extracellular signal-regulated kinase (ERK) and
p38 kinase and an inactivation of phosphatidylinositol 3-kinase
(PI3K)/Akt in a time-dependent manner. These findings provide evidence
demonstrating that the pro-apoptotic effect of fucoidan is mediated
through the activation of ERK, p38 and the blocking of the PI3K/Akt
signal pathway in HCT-15 cells. These data support the hypothesis that
fucoidan may have potential in colon cancer treatment.
Fucoidan induces apoptosis through activation of caspase-8 on human
breast cancer MCF-7 cells
www.ncbi.nlm.nih.gov...
Fucoidan is an active component of seaweed that has been shown to
inhibit proliferation and induce apoptotic cell death in several tumor
cells. However, the detailed mechanisms underlying this process have
not yet been elucidated. In the present report, we investigated the
effect of fucoidan on the induction of apoptosis in human breast
cancer MCF-7 cells. Our data demonstrated that fucoidan reduced the
viable cell number of MCF-7 cells in a dose- and time-dependent
manner. In contrast, fucoidan did not affect the viable cell number of
normal human mammary epithelial cells. Results from the apoptosis
assay demonstrated that fucoidan induced internucleosomal DNA
fragmentation, chromatin condensation, activation of caspase-7, -8,
and -9, and cleavage of poly(ADP ribose) polymerase.
Fucoidan Induces Apoptosis of Human HS-Sultan Cells (Leukemia)
http:/pubs.acs.org/doi/abs/10.1021/jf9010406
Fucoidan-induced apoptosis was accompanied by the activation of
caspase-3 and was partially prevented by pretreatment with a
pan-caspase inhibitor, Z-VAD-FMK. The mitochondrial potential in
HS-Sultan cells was decreased 24 hr after treatment with fucoidan,
indicating that fucoidan induced apoptosis through a mitochondrial
pathway. When HS-Sultan was treated with 100 mg/mL fucoidan for 24 hr,
phosphorylation of ERK and GSK markedly decreased. In contrast,
phosphorylation of p38 and Akt was not altered by treatment with
fucoidan. L-Selectin and P-selectin are known to be receptors of
fucoidan; however, as HS-Sultan does not express either of these
selectins, it is unlikely that fucoidan induced apoptosis through them
in HS-Sultan. The neutralizing antibody, Dreg56, against human
L-selectin did not prevent the inhibitory effect of fucoidan on the
proliferation of IM9 and MOLT4 cells, both of which express
L-selectin; thus it is possible fucoidan induced apoptosis though
different receptors. These results demonstrate that fucoidan has
direct anti-cancer effects on human HS-Sultan cells through caspase
and ERK pathways.
Fucoidan, a major component of brown seaweed, prohibits the growth of
human cancer cell lines in vitro
www.spandidos-publications.com...
The results revealed that cell proliferation was suppressed in 13 cell
lines in a time- and/or dose-dependent manner; this suppression was
marked in the hepatocellular carcinoma, cholangiocarcinoma and
gallbladder carcinoma cell lines. In contrast, proliferation of the
neuroblastoma and 1 of the 2 ovarian carcinoma cell lines was not
affected.
Inhibitory Effect of Fucoidan on Huh7 Hepatoma Cells (Liver Cancer)
Through Downregulation of CXCL12
www.britannica.com...
Western blotting revealed that the amount of α-fetoprotein was
decreased by 1.0 mg/ml of fucoidan in Huh7 cells, whereas it was
unchanged in HepG2 cells. In Huh7 cells, CXCL12 mRNA expression was
significantly downregulated by 1.0 mg/ml of fucoidan, whereas CXCR4
mRNA expression was unchanged by fucoidan. CXCL12 and CXCR4 mRNA were
barely expressed in HepG2 cells. In addition, 1.0 mg/ml of fucoidan
mildly arrested the cell cycle and induced apoptosis in Huh7 cells.
The findings suggest that fucoidan exhibits antitumor activity toward
Huh7 cells through the downregulation of CXCL12 expression.
Ethyl Alcohol Extracts of Hizikia fusiforme Sensitize AGS Human
Gastric Adenocarcinoma Cells (Bone Marrow Cancer)
www.liebertonline.com...
Resistance to tumor necrosis factor-related apoptosis-inducing ligand
(TRAIL)-induced apoptosis has been reported in some cancer cells,
including AGS human gastric adenocarcinoma cells. Hizikia fusiforme is
a commonly used brown seaweed species in Korea that possesses potent
antibacterial, antifungal, and anti-inflammatory activities. In this
study, we demonstrated that treatment with TRAIL in combination with
subtoxic concentrations of ethyl alcohol extract of H. fusiforme
(EAHF) sensitized TRAIL-resistant AGS cells to TRAIL-mediated
apoptosis. Combined treatment with EAHF and TRAIL increased chromatin
condensation, DNA fragmentation, and sub-G1-phase DNA content.
copyright & usage
reply posted on 22-8-2010 @ 03:25 PM by IgnoranceIsntBlisss
Genistein
Foods: Lupin (herb), Fava Beans, Soybeans, Kudzu, Psoralea, Coffee and
Flemingia Vestita (medicinal plant).
en.wikipedia.org...
Genistein-induced G2-M arrest, p21WAF1 upregulation, and apoptosis in
a non-small-cell lung cancer cell line
www.ncbi.nlm.nih.gov...
Our results showed that genistein can upregulate p21WAF1 expression in
genistein-treated cells. From these results, we conclude that
genistein may act as an anticancer agent, and further studies may
prove its efficacy in non-small lung cancer cells. Thus the biological
effects of genistein may, indeed, be due to the modulation of cell
growth, cell death, and cell cycle regulatory molecules.
Growth-inhibitory effects of the natural phyto-oestrogen genistein in
MCF-7 human breast cancer cells
www.ncbi.nlm.nih.gov...
The low incidence of breast cancer in countries with a flavonoid-rich
soy-based diet and the protection afforded by soy-derived products
against experimental mammary tumours in rats suggest that genistein
and other isoflavonoid compounds may exert an anti-tumour activity. We
analysed the effects of genistein on cell number and cell cycle
progression (flow cytometric analysis of propidium iodide-stained
nuclei) of human breast cancer cells (MCF-7) in vitro. Genistein
produced a significant, dose-dependent inhibition of MCF-7 cell growth
with an ID50 of approximately 40 microM after 72 h of incubation.
Genistein-induced upregulation of p21WAF1, downregulation of cyclin B,
and induction of apoptosis in prostate cancer cells
www.ncbi.nlm.nih.gov...
Here we report that genistein inhibits PCa cell growth in culture in a
dose-dependent manner, which is accompanied by a G2/M cell cycle
arrest. Cell growth inhibition was observed with concomitant
downregulation of cyclin B, upregulation of the p21WAF1
growth-inhibitory protein, and induction of apoptosis. Collectively,
these results provide experimental evidence for a novel effect of
genistein on cell cycle gene regulation, resulting in the inhibition
of cell growth and ultimate demise of tumor cells.
Genistein induces apoptosis and topoisomerase II-mediated DNA breakage
in colon cancer cells
www.ncbi.nlm.nih.gov...
The present study was undertaken to determine if (a) genistein induces
topo II-mediated DNA damage in HT-29 colon cancer cells; and (b) if
this damage is required to induce apoptosis. DNA damage was evaluated
using the comet assay. Apoptosis was determined by the ethidium
bromide/acridine orange staining technique. DNA breakage was noted
within 1 h of treatment. Apoptosis was only induced with high
concentrations (>/=60 microM) of genistein. Marked inhibition of HT-29
cell growth was evident at concentrations ranging from 60 to 150
microM. This was associated with a cell cycle arrest at G(2)/M.
Similar findings were obtained in SW-620 and SW-1116 colon cancer cell
lines. Aclarubicin, a topo II antagonist, reduced genistein-induced
DNA breaks but did not reduce apoptosis. These data suggest that, in
colon cancer cells, topo II serves as the enzymatic target of
genistein. Furthermore, topo II-mediated DNA cleavage is not required
for the induction of apoptosis.
The Potential of Soybean Foods as a Chemoprevention Approach for Human
Urinary Tract Cancer
clincancerres.aacrjournals.org...
Furthermore, both genistein and combined isoflavones exhibited a
significant tumor suppressor effect in vivo (P < 0.05). The results
justify the potential use of soybean foods as a practical
chemoprevention approach for patients with urinary tract cancer.
Prevention of metastatic pancreatic cancer growth in vivo by induction
of apoptosis with genistein, a naturally occurring isoflavonoid
www.ncbi.nlm.nih.gov...
In vivo, genistein significantly improved survival, almost completely
inhibited metastasis, and increased apoptosis in an orthotopic model
of pancreatic cancer. In vitro genistein treatment resulted in
apoptosis in all pancreatic cancer cell lines tested, and this
appeared to be mediated by activation of caspase-3.
Ginger
Food: Ginger Root.
en.wikipedia.org...
Related to Tumeric, it contains curcuminoids but also it's own other
unique cancer fighters.
Dietary ginger constituents, galanals A and B, are potent apoptosis
inducers in Human T lymphoma Jurkat cells
www.ncbi.nlm.nih.gov...
The effects of the constituents isolated from ginger species including
curcumin, 6-gingerol and labdane-type diterpene compounds on cell
proliferation and the induction of apoptosis in the cultured human T
lymphoma Jurkat cells were studied. Among the tested compounds,
galanals A and B, isolated from the flower buds of a Japanese ginger,
myoga (Zingiber mioga Roscoe), showed the most potent cytotoxic
effect. ...In conclusion, the results from this study provide
biological evidence that ginger-specific constituents other than
curcuminoids are potential anticancer agents.
Ginger ingredients reduce viability of gastric cancer cells via
distinct mechanisms
www.ncbi.nlm.nih.gov...
We found that 6-gingerol, a phenolic alkanone isolated from ginger,
enhanced the TRAIL-induced viability reduction of gastric cancer cells
while 6-gingerol alone affected viability only slightly. 6-Gingerol
facilitated TRAIL-induced apoptosis by increasing TRAIL-induced
caspase-3/7 activation. 6-Gingerol was shown to down-regulate the
expression of cIAP1, which suppresses caspase-3/7 activity, by
inhibiting TRAIL-induced NF-kappaB activation. As 6-shogaol has a
chemical structure similar to 6-gingerol, we also assessed the effect
of 6-shogaol on the viability of gastric cancer cells. Unlike
6-gingerol, 6-shogaol alone reduced the viability of gastric cancer
cells. 6-Shogaol was shown to damage microtubules and induce mitotic
arrest. These findings indicate for the first time that in gastric
cancer cells, 6-gingerol enhances TRAIL-induced viability reduction by
inhibiting TRAIL-induced NF-kappaB activation while 6-shogaol alone
reduces viability by damaging microtubules.
6-Shogaol (Alkanone from Ginger) Induces Apoptotic Cell Death of Human
Hepatoma p53
pubs.acs.org...
In conclusion, we provide here a novel modality that can help to
eradicate a p53 mutant of human hepatoma cells by using a natural
consistent isolated form of ginger. These data also provide evidence
to reaffirm the notion that consumption of certain foodstuffs can be
beneficial to health because some of the constituents contained in
them may be anticarcinogenic.
[size=3]Induction of apoptosis in HL-60 cells by pungent vanilloids,
[6]-gingerol and [6]-paradol[/size]
www.ncbi.nlm.nih.gov...
[6]-Paradol, another pungent phenolic substance found in ginger and
other Zingiberaceae plants, also has a vanilloid structure found in
other chemopreventive phytochemicals including curcumin. In the
present study, [6]-gingerol and [6]-paradol were found to exert
inhibitory effects on the viability and DNA synthesis of human
promyelocytic leukemia (HL-60) cells. The cytotoxic and
antiproliferative effects of both compounds were associated with
apoptotic cell death. The above results suggest that [6]-gingerol and
[6]-paradol possess potential cytotoxic/cytostatic activities.
Multiple mechanisms are involved in 6-gingerol-induced cell growth
arrest and apoptosis in human colorectal cancer cells
onlinelibrary.wiley.com...
The results suggest that 6-gingerol stimulates apoptosis through
upregulation of NAG-1 and G1 cell cycle arrest through downregulation
of cyclin D1. Multiple mechanisms appear to be involved in 6-gingerol
action, including protein degradation as well as β-catenin, PKCε, and
GSK-3β pathways.
Gingerol inhibits metastasis of MDA-MB-231 human breast cancer cells
www.ncbi.nlm.nih.gov...
In conclusion, we have shown that [6]-gingerol inhibits cell adhesion,
invasion, motility and activities of MMP-2 and MMP-9 in MDA-MB-231
human breast cancer cell lines.
Ginsenoside
Source: Ginseng Root.
en.wikipedia.org...
Anti-proliferative effect of ginseng saponins on human prostate cancer cell line
www.ncbi.nlm.nih.gov...
Ginseng is a medicinal herb widely used in Asian countries, and many
of its pharmacological actions are attributed to the ginsenosides. In
a study of the anti-proliferative activity of ginsenosides using human
prostate carcinoma LNCaP cell line, ginsenoside Rg3 displayed growth
inhibitory activity. The cells lost its adherent property after
incubation in the presence of 250 microM of ginsenoside for 48h.
[edit on 22-8-2010 by IgnoranceIsntBlisss]
copyright & usage
reply posted on 22-8-2010 @ 03:27 PM by IgnoranceIsntBlisss
An Intestinal Bacterial Metabolite of Ginseng Protopanaxadiol Saponins
Has the Ability to Induce Apoptosis in Tumor Cells
www.ncbi.nlm.nih.gov...
Our previous study demonstrated that the in vivo anti-metastatic
effect induced by oral administration of ginseng protopanaxadiol
saponins was mediated by their metabolic component M1, and that the
growth, invasion and migration of tumor cells were inhibited by M1 but
not by ginsenosides. Here we investigated the inhibitory mechanism of
M1 on the growth of tumor cells. M1 inhibited the proliferation of
B16-BL6 mouse melanoma cells in a time- and dose-dependent manner,
with accompanying morphological changes at the concentration of 20
microM. In addition, at 40 microM M1 induced apoptotic cell death
within 24 h. Fluorescence microscopy revealed that dansyl M1 entered
the cytosol and quickly reached the nuclei (approximately 15 min).
Western blot analysis revealed that M1 rapidly up-regulated the
expression of p27Kip1, but down-regulated the expression of c-Myc and
cyclin D1 in a time-dependent manner. Thus, the regulation of
apoptosis-related proteins by M1 is responsible for the induction of
apoptotic cell death, and this probably leads to the anti-metastatic
activity in vivo.
Antitumor activity of a novel ginseng saponin metabolite in human
pulmonary adenocarcinoma cells resistant to cisplatin
www.ncbi.nlm.nih.gov...
The in vitro antitumor activity of a novel ginseng saponin metabolite,
20-O-beta-D-glucopyranosyl-20(S)-protopanaxadiol (IH-901), was
examined against four human cancer cell lines and one subline
resistant to cisplatin (CDDP). The growth inhibitory activity of the
compound was estimated by MTT tetrazolium assay. The mean
concentrations of IH-901 needed to inhibit the proliferation of the
cells by 50% (IC50) were 24.3, 25.9, 56.6 and 24.9 microM against
human myeloid leukemia (HL-60), pulmonary adenocarcinoma (PC-14),
gastric adenocarcinoma (MKN-45) and hepatoma (HepG2) cell lines,
respectively. These values are higher than that of CDDP. In the
CDDP-resistant PC/DDP cell line, the IC50 values of IH-901 and CDDP
were 20.3 and 60.8 microM, respectively. These results suggest that
IH-901 is not cross-resistant to CDDP in this cell line and could be a
candidate for the treatment of CDDP resistant pulmonary cancer.
Grape Seed Extract
Surely you'll have to chew the seeds up if you want to be able to
digest the good stuff inside the seed.
Induction of Apoptosis in Human Leukemia Cells by Grape Seed Extract
Occurs via Activation of c-Jun NH2-Terminal Kinase
clincancerres.aacrjournals.org...
Conclusions: The result of the present study showed that GSE induces
apoptosis in Jurkat cells through a process that involves sustained
JNK activation and Cip1/p21 up-regulation, culminating in caspase
activation.
Grape seed extract induces apoptotic death of human prostate carcinoma
DU145 cells
carcin.oxfordjournals.org...
Together, these results suggest that GSE possibly causes mitochondrial
damage leading to cytochrome c release in cytosol and activation of
caspases resulting in PARP cleavage and execution of apoptotic death
of human PCA DU145 cells. Furthermore, GSE-caused caspase 3-mediated
apoptosis also involves other pathway(s) including caspase 9
activation.
Synergistic Anti-Cancer Effects of Grape Seed Extract and Conventional
Cytotoxic Agent Doxorubicin Against Human Breast Carcinoma Cells
www.springerlink.com...
In quantitative apoptosis studies, GSE and Dox alone and in
combination showed comparable apoptotic death of MCF-7 cells, however,
a combination of the two was inhibitory to Dox induced apoptosis in
MDA-MB468 cells. This was further confirmed in another estrogen
receptor-negative MDA-MB231 cell line, in which GSE and Dox
combination strongly inhibited cell growth but did not show any
increase in apoptotic cell death caused by Dox. Together, these
results suggest a strong possibility of synergistic efficacy of GSE
and Dox combination for breast cancer treatment, independent of
estrogen receptor status of the cancer cell.
Grape Seed Extract Induces Cell Cycle Arrest and Apoptosis in Human
Colon Carcinoma Cells
www.informaworld.com...=all~content=a905310312
We reported recently that GSE inhibits CRC cell HT29 growth in culture
and nude mice xenograft. Because GSE is available commercially through
different vendors, here we assessed whether GSE from 2 different
manufacturers produces comparable biological effects in a panel of
human CRC cell lines. Our results show that irrespective of source,
GSE strongly inhibits LoVo, HT29, and SW480 cell growth, with a G1
arrest in LoVo and HT29 cells but an S and/or G2/M arrest in SW480
cell cycle progression. GSE also induced Cip/p21 levels in all 3 cell
lines. Furthermore, an induction of apoptosis was observed in all 3
cell lines by GSE. Taken together, our findings suggest that GSE could
be an effective CAM agent against CRC possibly due to its strong
growth inhibitory and apoptosis-inducing effects.
Induction of apoptosis in HeLa cells by chloroform fraction of seed
extracts of Nigella sativa
www.cancerci.com...
Methanolic, n-Hexane and chloroform extracts of Nigella sativa seedz
effectively killed HeLa cells. The IC50 values of methanolic,
n-hexane, and chloroform extracts of Nigella sativa were 2.28 μg/ml,
2.20 μg/ml and 0.41 ng/ml, respectively. All three extracts induced
apoptosis in HeLa cells. Apoptosis was confirmed by DNA fragmentation,
western blot and terminal transferase-mediated dUTP-digoxigenin-end
labeling (TUNEL) assay. Western Blot and TUNEL results suggested that
Nigella sativa seed extracts regulated the expression of pro- and
anti- apoptotic genes, indicating its possible development as a
potential therapeutic agent for cervical cancer upon further
investigation.
High Fructose Corn Syrup (BAD)
List of foods that contain HFCS:
www.answerbag.com...
Cancer cells slurp up fructose, US study finds
www.reuters.com...
Pancreatic tumor cells use fructose to divide and proliferate, U.S.
researchers said on Monday in a study that challenges the common
wisdom that all sugars are the same. Tumor cells fed both glucose and
fructose used the two sugars in two different ways, the team at the
University of California Los Angeles found. They said their finding,
published in the journal Cancer Research, may help explain other
studies that have linked fructose intake with pancreatic cancer, one
of the deadliest cancer types. "These findings show that cancer cells
can readily metabolize fructose to increase proliferation," Dr.
Anthony Heaney of UCLA's Jonsson Cancer Center and colleagues wrote.
Hispolon
Food: Phellinus Linteus (Oriental Mushroom)
en.wikipedia.org...
Hispolon induces apoptosis in human gastric cancer cells
www.ncbi.nlm.nih.gov...
Severe side effects and complications such as gastrointestinal and
hematological toxicities because of current anticancer drugs are major
problems in the clinical management of gastric cancer, which
highlights the urgent need for novel effective and less toxic
therapeutic approaches. Hispolon, an active polyphenol compound, is
known to possess potent antineoplastic and antiviral properties.
...Furthermore, hispolon potentiated the cytotoxicity of
chemotherapeutic agents used in the clinical management of gastric
cancer. These results suggest that hispolon could be useful for the
treatment of gastric cancer either as a single agent or in combination
with other anticancer agents.
Hispolon from Phellinus linteus has antiproliferative effects via
MDM2-recruited ERK1/2 activity in breast and bladder cancer cells
www.ncbi.nlm.nih.gov...
The MDM2 proto-oncogene is overexpressed in many human tumors.
Although MDM2 inhibits tumor-suppressor function of p53, there exists
a p53-independent role for MDM2 in tumorigenesis. Therefore,
downregulation of MDM2 has been considered an attractive therapeutic
strategy. Hispolon extracted from Phellinus species was found to
induce epidermoid and gastric cancer cell apoptosis. ...The results
indicated that cells with higher ERK1/2 activity were more sensitive
to hispolon. In addition, hispolon-induced caspase-7 cleavage was
inhibited by the ERK1/2 inhibitor, U0126. In conclusion, hispolon
ubiquitinates and downregulates MDM2 via MDM2-recruited activated
ERK1/2. Therefore, hispolon may be a potential anti-tumor agent in
breast and bladder cancers.
Honey
en.wikipedia.org...
RAW honey is supposed to be the good stuff. The type of pollen the
bees used to make the honey is important.
copyright & usage
reply posted on 22-8-2010 @ 03:29 PM by IgnoranceIsntBlisss
Antineoplastic activity of honey in an experimental bladder cancer
implantation model: In vivo and in vitro studies
onlinelibrary.wiley.com...
In vitro studies revealed significant inhibition of the proliferation
of T24 and MBT-2 cell lines by 1–25% honey and of RT4 and 253J cell
lines by 6–25% honey. BrdU labeling index was significantly lower. FCM
showed lower S-phase fraction, as well as absence of aneuploidy
compared with control cells. In the in vivo studies, intralesional
injection of 6 and 12% honey as well as oral ingestion of honey
significantly inhibited tumor growth.
Bioactivity of Greek honey extracts on breast cancer (MCF-7), prostate
cancer (PC-3) and endometrial cancer (Ishikawa) cells
cat.inist.fr...
Thyme, pine and fir honey showed both antioestrogenic and a weak
oestrogenic effect at low and high concentration, respectively, in
MCF-7 cells. Thyme honey reduced the viability of Ishikawa and PC-3
cells, whereas fir honey stimulated the viability of MCF-7 cells. In
conclusion, Greek honeys are rich in phenolic compounds, they modulate
oestrogenic activity whereas a thyme honey-enriched diet may prevent
cancer-related processes in breast, prostate and endometrial cancer
cells.
Honey could help fight cancer
news.bbc.co.uk...
Honey and royal jelly could become part of the arsenal of weapons
against cancer, researchers say. A team from the University of Zagreb,
in Croatia, found a range of honey-bee products stopped tumours
growing or spreading in tests on mice. Writing in the Journal of the
Science of Food and Agriculture, they say human cancer sufferers may
also see benefits.
Isoliquiritigenin
Foods: Licorice, Shallots, Bean Sprouts.
Apoptosis Induced by Isoliquiritigenin in Human Gastric Cancer MGC-803 Cells
www.thieme-connect.com...
Isoliquiritigenin, which is possibly a principal anti-tumor
constituent of licorice, a traditional Chinese herb, was examined for
apoptosis-inducing activity in human gastric cancer MGC-803 cells.
...These results suggest that isoliquiritigenin induced apoptosis of
MGC-803 cells through calcium- and Deltapsi(m)-dependent pathways,
indicating that it is potentially useful as a natural anti-cancer
agent.
Isoliquiritigenin induces apoptosis by depolarizing mitochondrial
membranes in prostate cancer cells
www.aacrmeetingabstracts.org...
Isoliquiritigenin (ISL) is a simple chalcone derivative,
4,2',4'-trihydroxychalcone, found in licorice, shallot and bean
sprouts. It was reported to have chemoprotective effects; inhibitory
effects on murine colonic tumorigenesis, anti-angiogenic effect, and
apoptosis-inducing activity. ...The present results indicate that ISL
inhibits prostate cancer cell growth by decreasing DNA synthesis and
inducing apoptosis. The mechanism of apoptosis induction by ISL
probably involves a mitochondria / caspase-9-specific pathway for the
activation of the caspase cascade.
Isoliquiritigenin inhibits the proliferation and induces the apoptosis
of human non-small cell lung cancer a549 cells
www.ncbi.nlm.nih.gov...
Isoliquiritigenin (ISL) is a natural pigment with the simple chalcone
structure 4,2',4'-trihydroxychalcone. In the present study, we report,
for the first time, ISL-induced inhibition of the proliferation of the
human non-small cell lung cancer A549 cell line. 2. The results showed
that ISL not only inhibited A549 cell proliferation, but also induced
apoptosis and blocked cell cycle progression in the G1 phase.
Cyclooxygenase-2 plays a suppressive role for induction of apoptosis
in isoliquiritigenin-treated mouse colon cancer cells
www.ncbi.nlm.nih.gov...
Cellular damage induced by chronic inflammation is a well known cause
of colon carcinogenesis. Cyclooxygenase-2 (COX-2), the enzyme that
converts arachidonic acid to prostanoids, is known to play an
important role in inflammation. Herbal flavonoid isoliquiritigenin
(ILTG) has previously been reported to be a strong suppresser of the
COX-2 pathway as well as an inducer of apoptosis. Here we report that
the susceptibility to apoptosis by ILTG is dependent on the level of
COX-2 in mouse colon adenocarcinoma Colon 26, which spontaneously
expresses COX-2. This dependency was observed to be enhanced by
blockage of the lipoxigenases (LOXs)-mediated metabolic pathway and
attenuated by addition of a number of prostaglandins and thromboxanes.
Taken together, these findings indicate that ILTG-induced apoptosis is
negatively regulated by the COX-2 expression level.
Estrogenic and antiproliferative activities of isoliquiritigenin in
MCF7 breast cancer cells
www.ncbi.nlm.nih.gov...
Transfection experiments reveal that ISL is able to transactivate the
endogenous ER alpha in MCF7 cells and this is supported by the
capability to induce down-regulation of ER alpha protein levels and
up-regulation of pS2 mRNA. Moreover, by using chimeric proteins
consisting of the hormone binding domains of ER alpha and ER beta
fused to the Gal4 DNA binding domain, we have determined that ISL is
an estrogenic agonist of both ER isoforms. As a biological
counterpart, low and intermediate ISL concentrations that induce
substantial transcriptional activity stimulate the proliferation of
MCF7 cells. However, high levels of ISL become cytotoxic even in
steroid-receptor negative HeLa cells. Thus, the activity of ISL and
the balance between risk or chemopreventive factor for
estrogen-dependent breast cancer may depend on dietary intake.
Kaempferol
Foods: Tea, Broccoli, Grapefruit, Brussel Sprouts, Apples, Witch Hazel
en.wikipedia.org...
Kaempferol-induced growth inhibition and apoptosis in A549 lung cancer
cells is mediated by activation of MEK-MAPK
onlinelibrary.wiley.com...
To elucidate these mechanisms, we challenged human lung cancer cell
line A549 with kaempferol and investigated its effects upon cellular
growth and signal transduction pathways. Treatment of A549 cells with
kaempferol resulted in a dose- and time-dependent reduction in cell
viability and DNA synthesis with the rate of apoptosis equivalent to
0.9 ± 0.5, 5.2 ± 1.5, 16.8 ± 2.0, 25.4 ± 2.6, and 37.8 ± 4.5% on
treatment with 0, 17.5, 35.0, 52.5, and 70.0 μM kaempferol,
respectively.
Kaempferol sensitizes colon cancer cells to TRAIL-induced apoptosis
www.ncbi.nlm.nih.gov...
Kaempferol is a natural compound contained in edible plants, and tumor
necrosis factor-related apoptosis-inducing ligand (TRAIL) is a
promising anti-cancer agent. Here, we show for the first time that the
combined treatment with kaempferol and TRAIL drastically induced
apoptosis in human colon cancer SW480 cells, compared to single
treatments. Kaempferol markedly up-regulated TRAIL receptors, DR5 and
DR4. DR5 but not DR4 siRNA efficiently blocked apoptosis induced by
the co-treatment with kaempferol and TRAIL, indicating that DR5
up-regulation by kaempferol helps to enhance TRAIL actions. Moreover,
we examined the combined effect on normal human cells. The
co-treatment induced no apoptosis in normal human peripheral blood
mononuclear cells and little apoptosis in normal human hepatocytes.
These results suggest that kaempferol is useful for TRAIL-based
treatments for cancer.
Limonoids
Source: Citrus Peels.
en.wikipedia.org...
Differential Inhibition of Human Cancer Cell Proliferation by Citrus Limonoids
www.ncbi.nlm.nih.gov...
Limonoids have been shown to inhibit the growth of estrogen
receptor-negative and -positive human breast cancer cells in culture.
...The human cancer cell lines included leukemia (HL-60), ovary
(SKOV-3), cervix (HeLa), stomach (NCI-SNU-1), liver (Hep G2), and
breast (MCF-7). The growth-inhibitory effects of the four limonoids
and the limonoid glucoside mixture against MCF-7 cells were
significant, and the antiproliferative activity of the different
citrus limonoids was also dose and time dependent. No significant
effects were observed on growth of the other cancer cell lines treated
with the four individual limonoids at 100 μg/ml.
[edit on 22-8-2010 by IgnoranceIsntBlisss]
copyright & usage
reply posted on 22-8-2010 @ 03:31 PM by IgnoranceIsntBlisss
Citrus Limonoids Induce Apoptosis in Human Neuroblastoma Cells and
Have Radical Scavenging Activity
jn.nutrition.org...
Citrus limonoid glucosides, a family of fruit bioactive compounds,
were postulated to have free radical–scavenging and apoptosis-inducing
properties against certain types of cancers. Four highly purified
limonoid glucosides, limoin 17ß D-glucopypranoside (LG), obacunone 17ß
D-glucopyranoside (OG), nomilinic acid 17ß D-glucopyranoside (NAG),
and deacetylnomilinic acid 17ß D-glucopyranoside (DNAG) were tested
for superoxide radical (O2–)-quenching activity and cytotoxic action
against undifferentiated human SH-SY5Y neuroblastoma cells in culture.
All 4 scavenged O2– as measured by inhibition of pyrogallol
decomposition in a spectrophotometric assay. ...We conclude that
citrus limonoid glucosides are toxic to SH-SY5Y cancer cells.
Cytotoxicity is exerted through apoptosis by an as yet unknown
mechanism of induction. Individual limonoid glucosides differ in
efficacy as anticancer agents, and this difference may reside in
structural variations in the A ring of the limonoid molecule.
Citrus Reticulata blanco induces apoptosis in human gastric cancer cells SNU-668
www.ncbi.nlm.nih.gov...
Citrus fruits have been known to reduce the proliferation of many
cancer cells. The antiproliferative effects of Citrus reticulata
Blanco (CR) extract, the immature tangerine peel, on human gastric
cancer cell line SNU-668 were evaluated using
3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay,
4,6-diamidineo-2-phenylindole staining, terminal deoxynucleotidyl
transferase-mediated dUTP nick end labeling assay, reverse
transcription-polymerase chain reaction expressions of BCL-2, BAX and
CASP-3 genes, caspase-3 activity, and immunocytochemistry of
caspase-3. From the results of the morphological and biochemical
assays, CR (50 microg/ml) increased the apoptosis of human gastric
cancer cells with typical apoptotic characteristics, including
morphological changes of chromatin condensation and apoptotic body
formation.
Luteolin
Foods: Celery, Thyme, Dandelion, Rinds, Clover Blossum, Green Pepper,
Chamomile Tea, Olive Oil, Carrots, Sage, Peppermint, Rosemary, Perilla
and Oregano.
Antioxidant enzymes activity involvement in luteolin-induced human
lung squamous carcinoma CH27 cell apoptosis
www.ncbi.nlm.nih.gov...
Luteolin (3',4',5,7-tetrahydroxyflavone) is an active constituent of
Lonicera japonica (Caprifoliaceae), and has been reported to produce
anti-tumor activities. However, the apoptosis-inducing activity of
luteolin still remains unknown. Flavonoids have been found to possess
prooxidant and antioxidant action. The biological and pharmacological
effect of flavonoid may depend upon its behavior as either an
antioxidant or a prooxidant. Our experiments found that
luteolin-induced CH27 cell apoptosis was accompanied by activation of
antioxidant enzymes, such as superoxide dismutase and catalase, but
not through the production of reactive oxygen species and disruption
of mitochondrial membrane potential. Therefore, the effects of
luteolin on CH27 cell apoptosis were suspected to result from the
antioxidant rather than the prooxidant action of luteolin.
The combination of TRAIL and luteolin enhances apoptosis in human
cervical cancer HeLa cells
www.ncbi.nlm.nih.gov...
Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is one
of the most promising candidates for cancer therapeutics. However,
some tumor cells are resistant to TRAIL-induced apoptosis. Our
previous studies have shown that luteolin, a naturally occurring
flavonoid, induces the up-regulation of death receptor 5 (DR5), which
is a receptor for TRAIL. Here, we show for the first time that
luteolin synergistically acts with exogenous soluble recombinant human
TRAIL to induce apoptosis in HeLa cells, but not in normal human
peripheral blood mononuclear cells. The combined use of luteolin and
TRAIL induced Bid cleavage and the activation of caspase-8. Also,
human recombinant DR5/Fc chimera protein, caspase inhibitors, and DR5
siRNA efficiently reduced apoptosis induced by co-treatment with
luteolin and TRAIL. These results raise the possibility that this
combined treatment with luteolin and TRAIL might be promising as a new
therapy against cancer.
Effects of luteolin on the inhibition of proliferation and induction
of apoptosis in human myeloid leukaemia cells
www.ncbi.nlm.nih.gov...
Luteolin, a flavonoid isolated from the fruit of Vitex rotundifolia,
has been examined with regard to the inhibition of proliferation and
induction of apoptosis in human myeloid leukaemia HL-60 cells. The
concentration required for 50% inhibition of the growth after 96 h was
15 +/- 1.1 microM. The mode of cell death induced by luteolin was
found to be apoptosis, as judged by the morphologic alteration of the
cells and by the detection of DNA fragmentation using agarose gel
electrophoresis. The degree of apoptosis was quantified by a sandwich
enzyme immunoassay and flow cytometric analysis. These results suggest
that luteolin may be used as potential chemopreventive and
chemotherapeutic agents.
Induction apoptosis of luteolin in human hepatoma HepG2 cells
www.ncbi.nlm.nih.gov...
In addition, it showed that c-Jun NH2-terminal kinase (JNK) was
activated after the treatment of luteolin for 3-12 h. Further
investigation showed that a specific JNK inhibitor, SP600125, reduced
the activation of CPP 32, the mitochondrial translocation of Bax, as
well as the cytosolic release of cytochrome c that induced by
luteolin. Finally, the apoptosis induced by luteolin was suppressed by
a pretreatment with SP600125 via evaluating annexin V-FITC binding
assay. These data suggest that luteolin induced apoptosis via
mechanisms involving mitochondria translocation of Bax/Bak and
activation of JNK.
Luteolin inhibits insulin-like growth factor 1 receptor signaling in
prostate cancer cells
carcin.oxfordjournals.org...
Luteolin inhibited expression of cyclin D1 and increased expression of
p21. As a result, luteolin suppressed proliferation and induced
apoptosis of prostate cancer cells. Knockdown of IGF-1R by siRNA led
to inhibition of proliferation of prostate cancer cells. Results of in
vivo tumor growth assay indicated that luteolin inhibited PC-3 tumor
growth. Immunoblotting of the extracts of tumor tissues showed that
luteolin inhibited IGF-1R/AKT signaling. Our results provide a new
insight into the mechanisms that luteolin is against cancer cells.
Induction of cell cycle arrest and apoptosis in HT-29 human colon
cancer cells by the dietary compound luteolin
ajpgi.physiology.org...
We demonstrate that luteolin promotes both cell cycle arrest and
apoptosis in the HT-29 colon cancer cell line, providing insight about
the mechanisms underlying its antitumorigenic activities.
Luteolin Induces Apoptosis in Oral Squamous Cancer Cells
jdr.sagepub.com...
Results revealed that luteolin reduced the viability of SCC-4 cells
and induced apoptosis by decreasing the expression of cyclin-dependent
kinase (CDKs), cyclins, and phosphor- retinoblastoma (p-Rb)
anti-apoptotic protein, but increased the expression of pro-apoptotic
proteins and activated caspase 9 and 3, with a concomitant increase in
the levels of cleaved poly-ADP-ribose polymerase (PARP). Combination
treatment of luteolin with paclitaxel enhanced the cytotoxic effect of
paclitaxel in SCC-4 cells, and continuous administration of luteolin
suppressed the growth of xenograft tumors in nude mice. These results
suggest that luteolin could be an effective chemotherapeutic agent for
the treatment of oral squamous cell carcinoma.
Lycopene
Foods: Tomato, "Gac" Fruit, Red Carrot, Watermelon, Papaya, Red Algae,
Pink Guava and Grapefruit.
en.wikipedia.org...
It's what makes most (but not all) fruits and vegetable yellow-orange-red.
Lycopene Supplementation Inhibits Lung Squamous Metaplasia and Induces Apoptosis
cancerres.aacrjournals.org...
Higher intake of lycopene is related to a lower risk of lung cancer in
human studies. Lung cancer risk is associated with higher plasma
levels of insulin-like growth factor I (IGF-I) and/or lower levels of
IGF-binding protein 3 (IGFBP-3).
Lycopene interferes with...mammary cancer cells
www.ncbi.nlm.nih.gov...
Collectively, the above data suggest that the inhibitory effects of
lycopene on MCF7 cell growth are not due to the toxicity of the
carotenoid but, rather, to interference in IGF-I receptor signaling
and cell cycle progression.
copyright & usage
AboveTopSecret.com is advertising supported.
reply posted on 22-8-2010 @ 03:32 PM by IgnoranceIsntBlisss
Concentrations of Lycopene Induce Mitochondrial Apoptosis in LNCaP
Human Prostate Cancer Cells
ebm.rsmjournals.com...
Subsequently, we demonstrated that increasing concentrations of
lycopene significantly (P < 0.05) reduced mitochondrial transmembrane
potential, induced the release of mitochondrial cytochrome c, and
increased annexin V binding, confirming induction of apoptosis. Thus,
lycopene at physiologically relevant concentrations did not affect
cellular proliferation or promote necrosis but clearly altered
mitochondrial function and induced apoptosis in LNCaP human prostate
cancer cells.
A novel cleavage product formed by autoxidation of lycopene induces
apoptosis in HL-60 cells
www.ncbi.nlm.nih.gov...
We previously reported that an autoxidation mixture of lycopene
induced apoptosis in HL-60 human promyelocytic leukemia cells, but
lycopene alone did not. In the present study, bioassay-directed
fractionations of autoxidized lycopene led to isolation of a novel
cleavage product of lycopene. Spectral analyses elucidated its
structure as (E,E,E)-4-methyl-8-oxo-2,4,6-nonatrienal (MON),
suggesting the formation through the oxidative cleavages at the 5, 6-
and 13, 14-double bonds of lycopene.
Maitake D-Fraction
Source: Extract from Maitake Mushrooms.
en.wikipedia.org...
Possible disease remission in patient with invasive bladder cancer
with D-fraction regimen
www.ncbi.nlm.nih.gov...
This case study describes an invasive bladder cancer patient at a high
risk for disease recurrence who only followed a D-fraction regimen
(with vitamin C) refusing other medical interventions. The two-year
follow-up yet indicated no clinical evidence of progression of
residual disease or recurrence with possible disease remission.
Synergistic potentiation of interferon activity with maitake mushroom
d-fraction on bladder cancer cells
onlinelibrary.wiley.com...
The combination of IFN-2b (10 000 IU/mL) and PDF (200 µg/mL) reduced
growth by ≈75% in T24 cells. This appears to be due to a synergistic
potentiation of these two agents, inducing a G1 arrest with DNA-PK
activation. Therefore, the IFN-2b/PDF combination could trigger DNA-PK
activation that may act on the cell cycle to cease cancer cell growth.
Potential growth inhibitory effect of maitake D-fraction on canine cancer cells
www.ncbi.nlm.nih.gov...
The postulated anticancer effect of D-fraction, the bioactive extract
of maitake mushroom, on three types (CF33, CF21, and CL-1) of canine
cancer cells was evaluated. The effect of D-fraction on several human
cancer cells was also investigated. The effect of other beta-glucan
products was likewise examined. D-fraction was highly effective on the
canine cancer cells, either potently inhibiting cell growth or
directly killing cells. Similar effects were also demonstrated in
certain human cancer cells. However, other beta-glucan products
relevant to D-fraction had no such effects on canine cancer cells.
Therefore, D-fraction is a potent natural agent that could be useful
in treating canine cancers as well as other veterinary cancers.
Melatonin
Sold as a sleep aid. It is secreted by the pineal gland. Low melatonin
levels are associated with cancer, it's known to fight cancer, and it
helps chemotherapy patients endure the side effects.
en.wikipedia.org...
Melatonin and retinoic acid induces apoptosis in MCF-7 human breast cancer cells
www.springerlink.com...
These data suggest that the sequential treatment regimen of Mlt and
atRA may induce apoptosis by modulation of members of the Bcl-2 family
of proteins. Thus, this combinatorial regimen, which reduces the
concentration of atRA needed for clinical efficacy while enhancing its
anti-tumorigenic activity, could be of great therapeutic benefit, and
may, in fact, specifically induce the regression of established breast
tumors due to its apoptosis-promoting effects.
Decreased toxicity and increased efficacy of cancer chemotherapy using
the pineal hormone melatonin in metastatic solid tumour patients with
poor clinical status
www.ncbi.nlm.nih.gov...
Melatonin (MLT) has been proven to counteract chemotherapy toxicity,
by acting as an anti-oxidant agent, and to promote apoptosis of cancer
cells, so enhancing chemotherapy cytotoxicity. The aim of this study
was to evaluate the effects of concomitant MLT administration on
toxicity and efficacy of several chemotherapeutic combinations in
advanced cancer patients with poor clinical status. The study included
250 metastatic solid tumour patients (lung cancer, 104; breast cancer,
77; gastrointestinal tract neoplasms, 42; head and neck cancers, 27),
who were randomized to receive MLT (20 mg/day orally every day) plus
chemotherapy, or chemotherapy alone. ...This study indicates that the
pineal hormone MLT may enhance the efficacy of chemotherapy and reduce
its toxicity, at least in advanced cancer patients of poor clinical
status.
Melatonin induces apoptosis in human neuroblastoma cancer cells
www.ncbi.nlm.nih.gov...
Low concentrations (nanomolar) of melatonin had been previously shown
to inhibit cell proliferation in several cancer cell lines as well as
in experimental animal models. Additionally, cell growth inhibition
and differentiation of prostate cancer cell lines by high
concentrations (micromolar to millimolar) of melatonin have been
recently reported. In the present paper, we show the induction of
apoptosis by high doses of melatonin in the human neuroblastoma cell
line SK-N-MC. ...Treatment with 1 mm melatonin for 6 days induced cell
death in 75% of the cells. This novel finding shows that a nontoxic
natural indoleamine may be potential therapy for some types of human
neuroblastomas.
Melatonin and RZR/ROR receptor ligand CGP 52608 induce apoptosis in
the murine colonic cancer
www.ncbi.nlm.nih.gov...
The effects of melatonin and the thiazolinidinedione derivative CGP
52608 on apoptosis of Colon 38 cancer cells were investigated. Male
mice were implanted subcutaneously with a suspension of Colon 38
cells. Ten days after induction of tumors, the animals were treated
with melatonin or CGP 52608. Both substances were given in
subcutaneous injections in daily doses of 10 or 100 microg in the
evening for 6 days. The control group received solvent. The apoptotic
cells were visualized in paraffin sections by means of the
transferase-mediated dUTPnick end-labeling method. Both treatments
increased significantly and to the same degree the number of apoptotic
cells in tumors. This finding confirms our earlier observation that
melatonin exerts a pro-apoptotic effect on murine colonic cancer
cells. Moreover, because CGP 52608 is a ligand of RZR/ROR receptors
and the latter are considered by some investigators as nuclear binding
sites for melatonin, our data suggest the involvement of these
receptors in the pro-apoptotic effect of melatonin.
A randomized study of chemotherapy with cisplatin plus etoposide
versus chemoendocrine therapy with cisplatin, etoposide and the pineal
hormone melatonin as a first-line treatment of advanced non-small cell
lung cancer patients in a poor clinical state
onlinelibrary.wiley.com...
Recent studies suggest that the pineal hormone melatonin may reduce
chemotherapy-induced immune and bone marrow damage. In addition,
melatonin may exert potential oncostatic effects either by stimulating
host anticancer immune defenses or by inhibiting tumor growth factor
production. On this basis, we have performed a randomized study of
chemotherapy alone vs. chemotherapy plus melatonin in advanced
non-small cell lung cancer patients (NSCLC) with poor clinical status.
...The percent of 1-year survival was significantly higher in patients
treated with melatonin plus chemotherapy than in those who received
chemotherapy alone (15/34 vs. 7/36, P < 0.05). Finally, chemotherapy
was well tolerated in patients receiving melatonin, and in particular
the frequency of myelosuppression, neuropathy, and cachexia was
significantly lower in the melatonin group. This study shows that the
concomitant administration of melatonin may improve the efficacy of
chemotherapy, mainly in terms of survival time, and reduce
chemotherapeutic toxicity in advanced NSCLC, at least in patients in
poor clinical condition.
Methylselenocysteine
Foods: Garlic, Onions, Astralagus, Broccoli's, Radishes, Brussel
Sprouts, Ramps, Milk Vetch, Indian Mustard and Cabbage.
Sources: Health foods stores.
en.wikipedia.org...
Se-Methylselenocysteine (SeMSC) is a naturally occurring seleno-amino acid.
copyright & usage
reply posted on 22-8-2010 @ 03:34 PM by IgnoranceIsntBlisss
Se-Methylselenocysteine induces apoptosis through caspase activation
in HL-60 cells
carcin.oxfordjournals.org...
In our study, we found that Se-methylselenocysteine (MSC) induced
apoptosis through caspase activation in human promyelocytic leukemia
(HL-60) cells. Measurements of cytotoxicity, DNA fragmentation and
apoptotic morphology revealed that MSC was more efficient at inducing
apoptosis than selenite, but was less toxic. Moreover, MSC increased
both the apoptotic cleavage of poly(ADP-ribose) polymerase (PARP) and
caspase-3 activity, whereas selenite did not.
Se-methylselenocysteine inhibits phosphatidylinositol 3-kinase
activity of mouse mammary epithelial tumor cells
breast-cancer-research.com...
Se-methylselenocysteine (MSC), a naturally occurring selenium
compound, is a promising chemopreventive agent against in vivo and in
vitro models of carcinogen-induced mouse and rat mammary
tumorigenesis. We have demonstrated previously that MSC induces
apoptosis after a cell growth arrest in S phase in a mouse mammary
epithelial tumor cell model (TM6 cells) in vitro. The present study
was designed to examine the involvement of the phosphatidylinositol
3-kinase (PI3-K) pathway in TM6 tumor model in vitro after treatment
with MSC.
Selenocystine Induces S-Phase Arrest and Apoptosis in Human Breast
Adenocarcinoma MCF-7 Cells by Modulating ERK and Akt Phosphorylation
pubs.acs.org...
Selenocystine (SeC) is a nutritionally available selenoamino acid with
selective anticancer effects on a number of human cancer cell lines.
The present study shows that SeC inhibited the proliferation of human
breast adenocarcinoma MCF-7 cells in a time- and dose-dependent
manner, through the induction of cell cycle arrest and apoptotic cell
death.
Milk Thistle
en.wikipedia.org...
Milk thistle may limit liver damage from chemo
www.reuters.com...
An herb used since ancient times to treat liver ailments may help
reduce the liver damage caused by some cancer drugs, a study published
Monday suggests. In a study of 50 children undergoing chemotherapy for
acute lymphoblastic leukemia (ALL), researchers found that an herb
called milk thistle appeared to reduce treatment-related liver
inflammation.
Milk Thistle and Prostate Cancer
cancerres.aacrjournals.org...
Extracts from the seeds of milk thistle, Silybum marianum, are known
commonly as silibinin and silymarin and possess anticancer actions on
human prostate carcinoma in vitro and in vivo. Seven distinct
flavonolignan compounds and a flavonoid have been isolated from
commercial silymarin extracts.
Myricetin
Foods: Walnuts, Red Grapes, Berries, Onions, Bilberry and Southern
Bayberry shrub.
en.wikipedia.org...
MEK Inhibitor.
The effect of the flavonoids, quercetin, myricetin and epicatechin on
the growth and enzyme activities of MCF7 human breast cancer cells
www.ingentaconnect.com...
E and Q inhibited the O-deethylation of ethoxyresorufin (EROD)
catalysed by cytochrome P450 CYPIA. In contrast, M increased the EROD
reaction 2-fold. Q increased the activity of DT-diaphorase, NADPH
cytochrome c reductase and glutathione reductase, while E increased
only NADPH cytochrome c reductase activity. The effects on enzyme
activities in vitro suggest that there is not only the potential for
flavonoids to alter metabolic activation of carcinogens but also of
therapeutically administered drugs in vivo. We are at present
investigating the synergy between anti-cancer drugs and flavonoids in
terms of anti-tumour efficacy.
Myricetin is a novel natural inhibitor of neoplastic cell
transformation and MEK1
carcin.oxfordjournals.org...
Here we demonstrated that 3,3',4',5,5',7-hexahydroxyflavone
(myricetin), one of the major flavonols in red wine, is a novel
inhibitor of MEK1 activity and transformation of JB6 P+ mouse
epidermal cells. Myricetin (10 µM) inhibited
12-O-tetradecanoylphorbol-13-acetate (TPA) or epidermal growth factor
(EGF)-induced cell transformation by 76 or 72%, respectively, compared
with respective reductions of 26 or 19% by resveratrol (20 µM).
...Overall, these results indicated that myricetin has potent
anticancer-promoting activity and mainly targets MEK signaling, which
may contribute to the chemopreventive potential of several foods
including red wines.
Nikko Maple Bark
www.hort.uconn.edu...
Hot water extract of bark of Nikko maple (Acer nikoense) induces
apoptosis in leukemia cells
www.ncbi.nlm.nih.gov...
In screening for antitumor constituents in traditional crude drugs, we
used three cultured cell lines: mouse leukemia P388 cells,
doxorubicin-resistant P388 cells and leczyme (catalytic
lectin)-resistant P388 cells. The hot water extract (HWE) of the bark
of Nikko maple (Acer nikoense) showed concentration-dependent
inhibitory effects on the growth of these three cell lines. DNA
fragmentation and morphological changes, accompanied by condensed and
fragmented nuclei, were observed in the leukemia cell lines cultured
with HWE of the bark of Nikko maple. Treatment with this HWE increased
the expression of sialylated glycoconjugates on the apoptotic cells.
These results suggest that HWE induces cell death via apoptosis in
vitro.
Nurture
en.wikipedia.org...
While medical sources typically claim that methods such as massage
therapy lacks scientific data in healing, common sense and scientific
data might say otherwise. Consider neglected children who don't
properly develop, how depression can shorten lifespans and sex
increases the size and health of the brain.
www.mayoclinic.com...
While more research is needed to confirm the benefits of massage, some
studies have found massage helpful for: Stress relief, Managing
anxiety and depression, Pain, Stiffness, Blood pressure control,
Infant growth, Sports-related injuries, Boosting immunity and Cancer
treatment.
drfreire.com...
The child may have been born healthy but if he is exposed to toxins
such as lead or alcohol, physical abuse and neglect and other
childhood traumas, may develop abnormally, have stunted growth and
serious problems in later life.
en.wikibooks.org...
When children lack physical contact or nurturing, psycho-social
dwarfism may impede their growth. The hypothalamus does not stimulate
the thyroid to produce enough growth hormone. In studies on Romanian
orphanage children, the orphans had stunted growth, lower IQs, and
more learning disabilities than average children (Groza et al., 1998).
A few years after the orphans were adopted, they caught up in height
and improved their learning abilities.
serendip.brynmawr.edu...
An excessively active sympathetic nervous system may inhibit growth
hormone secretion. Researchers have attempted to pinpoint the
importance of this factor in psychogenic dwarfism by injecting a drug
that blocks one part of the sympathetic nervous system. Studies have
indicated that this causes an increase in growth hormone levels that
eventually return to normal. Additionally, glucocorticoids play a
factor. Glucocorticoids are steroid hormones that act similarly to
epinephrine and serve to energize the body during periods of stress;
however, unlike epinephrine that acts within seconds, glucocorticoids
work over a period of hours. This suggests that perhaps
glucocorticoids act to help the body recover after a stressor, or
prepare for the next stressor, rather than mediating the stress
response. Not surprisingly, some children with psychogenic dwarfism
display high levels of glucocorticoids. This effect is also seen in
rats that have been deprived of their mothers. Glucocorticoids block
the secretion of the growth hormone, the reception of growth hormones
by the target cells, and the synthesis of new proteins and new DNA in
dividing cells.
news.medill.northwestern.edu...
African-American life expectancy on average is seven to eight years
less than non-Hispanic white Americans according to the Centers for
Disease Control, but blacks are also far less likely to self-report
major depression and anxiety. Does that mean African-Americans are
living shorter, yet happier lives? The answer to that question is no,
according to the University of Michigan's Director of the Institute of
Social Research, Dr. James Jackson.
www.livescience.com...
Sex apparently can help the brain grow, according to new findings in
rats. Sexually active rodents also seemed less anxious than virgins,
Princeton scientists discovered. Past findings had shown that
stressful, unpleasant events could stifle brain cell growth in adults.
To see if pleasant albeit stressful experiences could have the
opposite effect, researchers studied the effects of sex in rats.
copyright & usage
reply posted on 22-8-2010 @ 03:36 PM by IgnoranceIsntBlisss
Olives & Olive Oil
en.wikipedia.org...
Epidermal growth factor receptor inhibition is proven to stop many
forms and instances of cancer. There are numerous commerical forms of
medicine out there, but if you even need such measures is up to
professionals. Olive's possess natural EGFR Inhibitors.
Cancer chemoprevention by hydroxytyrosol isolated from virgin olive
oil through G1 cell cycle arrest and apoptosis
www.ncbi.nlm.nih.gov...
Recent epidemiological evidence and animal studies suggest a
relationship between the intake of olive oil and a reduced risk of
several malignancies. ...The con-centrations of hydroxytyrosol which
inhibited 50% of cell proliferation were ∼50 and ∼750 μmol/l for HL60
and both HT29 and HT29 clone 19A cells, respectively. At
concentrations ranging from 50 to 100 μmol/l, hydroxytyrosol induced
an appreciable apoptosis in HL60 cells after 24 h of incubation as
evidenced by flow cytometry, fluorescence microscopy and
internucleosomal DNA fragmentation. ... These results support the
hypothesis that hydroxytyrosol may exert a protective activity against
cancer by arresting the cell cycle and inducing apoptosis in tumour
cells, and suggest that hydroxytyrosol, an important component of
virgin olive oil, may be responsible for its anticancer activity.
Olive Fruit Extracts Inhibit Proliferation and Induce Apoptosis in
HT-29 Human Colon Cancer Cells
jn.nutrition.org...
We investigated the effect on cell proliferation and apoptosis in
HT-29 cells of an extract from the skin of olives composed of
pentacyclic triterpenes with the main components maslinic acid
(73.25%) and oleanolic acid (25.75%). Studies of the dose-dependent
effects showed antiproliferative activity at an EC50 value of 73.96 ±
3.19 µmol/L of maslinic acid and 26.56 ± 2.55 µmol/L of oleanolic acid
without displaying necrosis. Apoptosis was confirmed by the
microscopic observation of changes in membrane permeability in 40.9 ±
3.9% and detection of DNA fragmentation in 24.5 ± 1.5% of HT-29 cells
incubated for 24 h with olive fruit extract containing 150 and 55.5
µmol/L of maslinic and oleanolic acids, respectively.
Olive oils bitter principle reverses acquired autoresistance to
trastuzumab (Herceptin™) in HER2-overexpressing breast cancer cells
www.biomedcentral.com...
A low incidence of breast cancer in the Mediterranean basin suggests
that a high consumption of Extra Virgin Olive Oil (EVOO) might confer
this benefit. ...Mechanistically, oleuropein aglycone treatment
significantly reduced HER2 ECD cleavage and subsequent HER2
auto-phosphorylation, while it dramatically enhanced Tzb-induced
down-regulation of HER2 expression. ...Olive oil's bitter principle
(i.e., oleuropein aglycone) is among the first examples of how
selected nutrients from an EVOO-rich "Mediterranean diet" directly
regulate HER2-driven breast cancer disease.
Oridonin
Source: Rabdosia Rubescens Plant.
medical-dictionary.thefreedictionary.com...
Oridonin, a diterpenoid purified from Rabdosia rubescens, inhibits the
proliferation of cells from lymphoid malignancies
mct.aacrjournals.org...
This study found that oridonin, a natural diterpenoid purified from
Rabdosia rubescens, inhibited growth of multiple myeloma (MM; U266,
RPMI8226), acute lymphoblastic T-cell leukemia (Jurkat), and adult
T-cell leukemia (MT-1) cells with an effective dose that inhibited 50%
of target cells (ED50) ranging from 0.75 to 2.7 μg/mL.
Autophagy preceded apoptosis in oridonin-treated human breast cancer MCF-7 cells
www.ncbi.nlm.nih.gov...
Recent studies have shown that MCF-7 cells undergo autophagy under
some conditions, such as tamoxifen treatment and starvation. In this
study, we investigated autophagy in MCF-7 cells under oridonin
treatment and further examined the relationship between autophagy and
apoptosis. After 3-MA (the specific inhibitor of autophagy)
pre-culture, MCF-7 cells were exposed to oridonin, and the growth
inhibitory ratio, morphologic changes, DNA fragmentation, proteins
expression, autophagic ratio and apoptotic ratio were evaluated.
Oridonin inhibited the proliferation of MCF-7 cells and induced
autophagy in vitro.
Oridonin-treated MCF-7 human breast cancer cells
onlinelibrary.wiley.com...
Oridonin inhibited cell growth in a time- and dose-dependent manner.
Cell cycle was altered through the upregulation of p53 and p21 protein
expressions. Pancaspase inhibitor Z-VAD-fmk and calpain inhibitor II
both decreased cell death ratio.
Oyster Sauce (BAD)
en.wikipedia.org...
In 2001 the United Kingdom Food Standards Agency found in tests of
various oyster sauces and soy sauces that some 22% of samples
contained a chemical called 3-MCPD (3-monochloropropane-1,2-diol) at
levels considerably higher than those deemed safe by the European
Union. About two-thirds of these samples also contained a second
chemical called 1,3-DCP (1,3-dichloropropane-2-ol) which experts
advise should not be present at any levels in food. Both chemicals
have the potential to cause cancer and the Agency recommended that the
affected products be withdrawn from shelves and avoided.[12][13]
Paclitaxel
Source: Pacific Yew Tree (Taxus brevifolia)
en.wikipedia.org...
This is the natural version of a highly used chemotherapy drug known
as Taxol. It has well known effectiveness against multiple lines of
cancer and citations shouldn't be necessary.
Pepino Melon
Source: Fruits from Solanum Muricatum.
en.wikipedia.org...
Extract of Solanum muricatum (Pepino/CSG) inhibits tumor growth by
inducing apoptosis
www.ncbi.nlm.nih.gov...
A lyophilized aqueous fraction extracted from Solanum muricatum (CSG4)
was used in this study. The human cell lines tested include: prostate
(PC3, DU145), stomach (MKN45), liver (QGY-7721, SK-HEP-1), breast
(MDA-MB-435), ovarian (OVCAR), colon (HT29) and lung (NCI-H209) cancer
cells; NHP (prostate), HUVEC (umbilical vein endothelial cell), and
WI-38 (lung diploid fibroblasts) normal cells. The cell survival was
determined by either Cell Titer MTS cell proliferation kit or trypan
blue dye exclusion assay. The apoptosis was analyzed by (a) apoptotic
morphology by light microscopy; (b) DNA ladder formation; (c) PARP
cleavage assay. Taken together, the present study suggests, for the
first time, that CSG may represent promising new chemical entity which
preferentially targets various tumor cells by triggering apoptosis.
Pinellia
Source: Root called "Ban Xia" used in Chinese Medicine to transform
phlegm and stop coughing.
en.wikipedia.org...
Apoptosis induction effect of Pinellia extract fraction on cell lines
of cervical cancer cultured in vitro
en.cnki.com.cn...
We tested the effects of PE on cell proliferation by MTT assay.The
effects of PE on morphology,and cell cycle were studied by
phase-contrast microscope and fiowcytometry(FCM).Results: PE could
obviously inhibit the proliferation of HeLa and CaSki cells in a time
and dose dependent manner.It could induce apoptosis of HeLa and
CaSki.Conclusions: PE can suppress proliferation of cervical cancer
cells and induce apoptosis.It may be a pure traditional Chinese
reagent with non-side effects to prevent and treat cervical cancer
effectively.
Experimental study on Inducing apoptosis effects of the protein of
Pinellia pedatisecta Schott on human ovarian cancer cell line SKOV3
en.cnki.com.cn...
OBJECTIVE To investigate the effects of the protein of Pinellia
pedatisecta Schott on the proliferation of human ovarian cancer cell
line SKOV3 in vitro and to determine whether the protein of Pinellia
pedatisecta Schott inhibit the growth of ovarian cancer and its
mechanism of action.METHODS CCK-8 was used to detect the effect of the
protein of Pinellia pedatisecta Schott on the growth of SKOV3 cells in
vitro;using flow cytometry,detected the apoptosis of SKOV3 cells
treated with the protein of Pinellia pedatisecta Schott by
Anexinn-V.RESULTS The protein of Pinellia pedatisecta Schott had some
effect of inhibiting the proliferation and inducing apoptosis of SKOV3
cells,and the mechanism would be further studied.
Revised Pinellia Combination Treat Digestive Tract Reaction from
Chemical Therapy after Operation of Gastric Cancer
en.cnki.com.cn...
The patients were randomly divided into two groups as study
subjects,the treatment group(n=39) were treated with revised Pinellia
Combination,5-Fu,Adriamycin and Mitomycin; while the control(n=44)
with 5-Fu,Adriamycin and Mitomycin. [Result] The treatment group had
much less reactions of nausea,vomiting and anorexia than
control(P0.05).
[edit on 22-8-2010 by IgnoranceIsntBlisss]
copyright & usage
reply posted on 22-8-2010 @ 03:39 PM by IgnoranceIsntBlisss
Polyphenols
Foods: Berries, Tea, Beer, Grapes/Wine, Olive Oil, Chocolate/Cocoa,
Coffee, Walnuts, Peanuts, Borojo, Pomegranates, Popcorn, Yerba Mate
and other fruits & vegetables.
en.wikipedia.org...
en.wikipedia.org...
Polyphenols are a group of important antioxidants. Citations proving
they kill cancer would be endless so are therefore pointless, but
several of the entires in here are polyphenols.
Polysaccharides
Source: "Turkey Tail" Mushroom (Trametes versicolor), Ginko Biloba
plant & seeds, Marine algae Capsosiphon Fulvescens and the "loach"
fish Misgurnus Anguillicaudatus.
en.wikipedia.org...
Protein-bound polysaccharide K induced apoptosis of the human Burkitt
lymphoma cell line, Namalwa
www.ncbi.nlm.nih.gov...
Protein-bound polysaccharide K (PSK), which is derived from mushrooms
belonging to the Basidiomycetes genus, has been clinically used as a
biological response modifier (BRM) for the treatment of epithelial
cancer patients in Japan and other Asian countries. There are a large
number of studies on the biological activities of PSK as regards the
activation of immunocompetent cells and the potential cytotoxic
effects on epithelial cancer cells. ...These results provide initial
evidence of the direct cytotoxic activity of PSK in a hematological
malignant cell line, thus encouraging further molecular-level study of
PSK-mediated apoptosis in malignant hematological cells.
Gene expression in response to anti-tumour intervention by
polysaccharide-K (PSK) in colorectal carcinoma cells
www.ncbi.nlm.nih.gov...
Distant metastasis is one of the major problems in treatment for
advanced colorectal cancer. Polysaccharide-K (PSK), or Krestin, a
mushroom ingredient, has been used as a chemoimmunotherapeutic agent
for the treatment of cancers in Asia for over 30 years. Some studies
have reported that PSK prevent distant metastases and improve survival
rates by 10-20% in colorectal cancer.
A polysaccharide of the marine alga Capsosiphon fulvescens induces
apoptosis in AGS gastric cancer cells
www.ncbi.nlm.nih.gov...
Because seaweed extracts have recently been found to have antioxidant
and anti-tumor activities, we analyzed a hot-water-soluble
polysaccharide (PS) of the marine alga Capsosiphon fulvescens for its
potential as a functional foodstuff by determining its effects on cell
growth and DNA synthesis. MTS assays showed that the C. fulvescens PS
(Cf-PS) significantly inhibited the proliferation of cultured human
cancer cells in a dose-dependent manner. Cf-PS-treated AGS cells
exhibited a marked increase in caspase-3 activation and a decrease in
Bcl-2 expression. In addition, phosphorylation of insulin-like growth
factor-I receptor (IGF-IR) was decreased in Cf-PS-treated AGS cells as
compared to non-treated control cells, which is consistent with
PI3-kinase (PI3K)/Akt activation. Cf-PS also decreased
IGF-I-stimulated recruitment of p85 to IGF-IR and IRS-1. These results
indicate that Cf-PS inhibits cell proliferation and induces apoptosis
by inhibiting IGF-IR signaling and the PI3K/Akt pathway.
Therapeutic mechanism of ginkgo biloba exocarp polysaccharides on gastric cancer
www.ncbi.nlm.nih.gov...
Compared with the statement before treatment, GBEP capsules could
reduce the area of tumors, and the effective rate was 73.4%.
Ultrastructural changes of the cells indicated that GBEP could induce
apoptosis and differentiation in tumor cells of patients with gastric
cancer. GBEP could inhibit the growth of human gastric cancer SGC-7901
cells following 24-72 h treatment in vitro at 10-320 mg/L, which was
dose- and time-dependent. GBEP was able to elevate the apoptosis rate
and expression of c-fos gene, but reduce the expression of c-myc and
bcl-2 genes also in a dose-dependent manner.
Apoptosis of hepatoma cells SMMC-7721 induced by Ginkgo biloba seed
polysaccharide
www.ncbi.nlm.nih.gov...
GBSP product obtained was of high purity with the average molecular
weight of 1.86 X 10(5). Quantitative analysis of SMMC-7721 cells in
vitro with FCM showed that the percentages of G(2)-M cells without and
with GBSP treatment were 17.01+/-1.28 % and 11.77+/-1.50% (P<0.05),
the debris ratio of the cells were 0.46+/-0.12 % and 0.06+/-0.06 %
(P<0.01), and the apoptosis ratio of cells was 3.84+/-0.55 % and
9.13+/-1.48 % (P<0.01) respectively. Following GBSP treatment,
microvilli of SMMC-7721 cells appeared thinner and the number of
spherical cells increased markedly. Most significantly, the apoptosis
bodies were formed on and around the spherical cells treated with
GBSP.
Mechanism of apoptosis induced by a polysaccharide, from the loach
Misgurnus anguillicaudatus (MAP) in human hepatocellular carcinoma
cells
www.ncbi.nlm.nih.gov...
The biological activities of the polysaccharide have attracted more
and more attention in the biochemical and medical areas due to their
anti-cancer effects. To estimate the anti-tumor mechanism of MAP, a
novel polysaccharide from the loach, Misgurnus anguillicaudatus, the
apoptosis effects of the polysaccharide on the human hepatocellular
carcinoma cells (SMMC-7721 cells) were studied. The present studies
showed that MAP could induce cell apoptosis which was closely
accompanied with an increase of intracellular-free calcium
concentration ([Ca2+]i), the enhancement of reactive oxygen species
(ROS) level, dissipation of mitochondria membrane potential (MMP),
up-regulation of p53 mRNA, increase expression of Bax mRNA, and
decrease expression of Bcl-2 mRNA. These results suggested that cell
apoptosis induced by MAP mainly was mediated by mitochondrial
pathways, not involved death receptors (DRs) pathways. The mechanism
possibly is that MAP acts on mitochondria and boosts ROS, ROS mediates
a release of Ca2+ from the intracellular Ca2+ pool, increasing [Ca2+]i
targets the cells a start-up of the apoptosis program.
Protodioscin
Food: Fenugreek (aka Methi) Seeds / Powder.
Sources: Indian markets.
en.wikipedia.org...
These seeds are very hard, and I suggest you buy powder instead. I
planted some out of my spice cabinet that were probably 10 years old
and they all sprouted.
Protodioscin isolated from fenugreek induces cell death and
morphological change indicative of apoptosis in leukemic cell line
H-60, but not in gastric cancer cell line KATO III.
www.ncbi.nlm.nih.gov...
Protodioscin (PD) was purified from fenugreek (Trigonella
foenumgraecum L.) and identified by Mass, and 1H- and 13C-NMR. The
effects of PD on cell viability in human leukemia HL-60 and human
stomach cancer KATO III cells were investigated. PD displayed strong
growth inhibitory effect against HL-60 cells, but weak growth
inhibitory effect on KATO III cells.
Methyl protodioscin induces G2/M cell cycle arrest and apoptosis in
HepG2 liver cancer cells
www.ncbi.nlm.nih.gov...
Methyl protodioscin (NSC-698790) is one of the main bioactive
components in the traditional Chinese medicine Dioscorea collettii
var. hypoglauca (Dioscoreaceae). In this study, we investigated the
anti-proliferative effect of methyl protodioscin on the HepG2 cells
and the mechanism of the induced cytotoxicity. Treatment of methyl
protodioscin resulted in G2/M arrest and apoptosis in HepG2 cells.
These effects were attributed to down-regulation of Cyclin B1 and the
signaling pathways leading to up-regulation of Bax and down-regulation
of BCL2, suggesting that methyl protodioscin may be a novel
anti-mitotic agent.
Methyl protodioscin induces G2/M arrest and apoptosis in K562 cells
www.ncbi.nlm.nih.gov...
Methyl protodioscin is a furostanol bisglycoside with antitumor
properties. The present study investigated its effects on human
chronic myelogenous leukemia K562 cells. Cell cycle analysis showed
that methyl protodioscin caused distinct G2/M arrest, with the
appearance of polyploidy population.
Punicalagin
Food: Pomegranate.
en.wikipedia.org...
In vitro antiproliferative, apoptotic and antioxidant activities of
punicalagin, ellagic acid and a total pomegranate tannin extract are
enhanced in combination with other polyphenols as found in pomegranate
juice
www.plefa.com...(05)00019-7/abstract
The potent antioxidant and anti-atherosclerotic activities of PJ are
attributed to its polyphenols including punicalagin, the major fruit
ellagitannin, and ellagic acid (EA). Punicalagin is the major
antioxidant polyphenol ingredient in PJ. Punicalagin, EA, a
standardized total pomegranate tannin (TPT) extract and PJ were
evaluated for in vitro antiproliferative, apoptotic and antioxidant
activities. Punicalagin, EA and TPT were evaluated for
antiproliferative activity at 12.5–100 μg/ml on human oral (KB,
CAL27), colon (HT-29, HCT116, SW480, SW620) and prostate (RWPE-1,
22Rv1) tumor cells. ...Pomegranate juice showed greatest
antiproliferative activity against all cell lines by inhibiting
proliferation from 30% to 100%. At 100 μg/ml, PJ, EA, punicalagin and
TPT induced apoptosis in HT-29 colon cells.
copyright & usage
<< 1 2 >> Part two continues, refer to:
http://www.abovetopsecret.com/forum/cancerisdead.html
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
WARNING FROM RAEL: For those who don't use their intelligence at its full
capacity, the label "selected by RAEL" on some articles does not mean that I
agree with their content or support it. "Selected by RAEL" means that I believe
it is important for the people of this planet to know about what people think or
do, even when what they think or do is completely stupid and against our
philosophy. When I selected articles in the past about stupid Christian
fundamentalists in America praying for rain, I am sure no Rael-Science reader
was stupid enough to believe that I was supporting praying to change the
weather. So, when I select articles which are in favor of drugs, anti-semitic,
anti-Jewish, racist, revisionist, or inciting hatred against any group or
religion, or any other stupid article, it does not mean that I support them. It
just means that it is important for all human beings to know about them. Common
sense, which is usually very good among our readers, is good enough to
understand that. When, like in the recent articles on drug decriminalization, it
is necessary to make it clearer, I add a comment, which in this case was very
clear: I support decriminalizing all drugs, as it is stupid to throw depressed
and sad people (as only depressed and sad people use drugs) in prison and ruin
their life with a criminal record. That does not mean that there is any change
to the Message which says clearly that we must not use any drug except for
medical purposes. The same applies to the freedom of expression which must be
absolute. That does not mean again of course that I agree with anti-Jews,
antisemites, racists of any kind or anti-Raelians. But by knowing your enemies
or the enemies of your values, you are better equipped to fight them. With love
and respect of course, and with the wonderful sentence of the French philosopher
Voltaire in mind: "I disapprove of what you say, but I will defend to the death
your right to say it".
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
"Ethics" is simply a last-gasp attempt by deist conservatives and
orthodox dogmatics to keep humanity in ignorance and obscurantism,
through the well tried fermentation of fear, the fear of science and
new technologies.
There is nothing glorious about what our ancestors call history,
it is simply a succession of mistakes, intolerances and violations.
On the contrary, let us embrace Science and the new technologies
unfettered, for it is these which will liberate mankind from the
myth of god, and free us from our age old fears, from disease,
death and the sweat of labour.
Rael
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