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05-01-2012, 11:48 AM
Study: Cannabinoid Reduces Breast Cancer Cell Aggression
Saturday, November 24 2007 @ 12:31 AM EST
Edited by: Michael Hess
Cannabidiol may be helpful in reducing the aggressiveness of breast cancer cells
BBSNews 2007-11-24 -- (IACM) In a mouse model of metastatic breast cancer the natural non- psychotropic cannabinoid cannabidiol (CBD) reduced the aggressiveness of breast cancer cells.
CBD inhibited a protein called Id-1. Id proteins play an important role in tumour cell biology. The researchers of the California Pacific Medical Center Research Institute concluded that "CBD represents the first nontoxic exogenous agent that can significantly decrease Id- 1 exp<b></b>ression in metastatic breast cancer cells leading to the down-regulation of tumor aggressiveness."
The authors stressed that they were not suggesting patients smoke cannabis. They added that it would be highly unlikely that effective concentrations of CBD could be reached by smoking cannabis. Lead researcher Dr. Sean McAllister said: "Right now we have a limited range of options in treating aggressive forms of cancer. Those treatments, such as chemotherapy, can be effective but they can also be extremely toxic and difficult for patients. This compound offers the hope of a non-toxic therapy that could achieve the same results without any of the painful side effects."
(Sources: BBC News of 19 November 2007; McAllister SD, Christian RT, Horowitz MP, Garcia A, Desprez PY. Cannabidiol as a novel inhibitor of Id-1 gene exp<b></b>ression in aggressive breast cancer cells. Mol Cancer Ther 2007;6(11):2921-7.)
source: http://bbsnews.net/a...071124003153693
The endogenous cannabinoid anandamide inhibits human breast cancer cell proliferation
Luciano De Petrocellis*,, Dominique Melck*,, Antonella Palmisano, Tiziana Bisogno, Chiara Laezza, Maurizio Bifulco, and Vincenzo Di Marzo,
+Author Affiliations
Istituto di Cibernetica and Istituto per la Chimica di Molecole di Interesse Biologico (affiliated with the National Institute for the Chemistry of Biological Systems, Consiglio Nazionale delle Ricerche), Consiglio Nazionale delle Ricerche, Via Toiano 6, 80072 Arco Felice, Naples, Italy; Istituto di Ricerche sullAdattamento dei Bovini e dei Bufali allAmbiente del Mezzogiorno, Consiglio Nazionale delle Ricerche, Ponticelli, 80147 Naples, Italy; and Centro di Studio der lEndocrinologia e lOncologia Sperimentale, Consiglio Nazionale Delle Richerche and Dipartimento di Biologia e Patologia Cellulare e Molecolare, Universit di Napoli Federico II, 80131 Naples, Italy
Communicated by Rita Levi-Montalcini, Institute of Neurobiology, Consiglio Nazionale delle Ricerche, Rome, Italy (received for review March 6, 1998)
Abstract
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 M and 8392% maximal inhibition at 510 M. The proliferation of several other nonmammary tumoral cell lines was not affected by 10 M 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. A stable analogue of anandamide -methanandamide, another endogenous cannabinoid, 2-arachidonoylglycerol, and the synthetic cannabinoid HU-210 also inhibited EFM-19 cell proliferation, whereas arachidonic acid was much less effective. These cannabimimetic substances displaced the binding of the selective cannabinoid agonist [3H]CP 55,940 to EFM-19 membranes with an order of potency identical to that observed for the inhibition of EFM-19 cell proliferation. Moreover, anandamide cytostatic effect was inhibited by the selective CB1 receptor antagonist SR 141716A. Cell proliferation was arrested by a prolactin mAb and enhanced by exogenous human prolactin, whose mitogenic action was reverted by very low (0.10.5 M) doses of anandamide. Anandamide suppressed the levels of the long form of the prolactin receptor in both EFM-19 and MCF-7 cells, as well as a typical prolactin-induced response, i.e., the exp<b></b>ression of the breast cancer cell susceptibility gene brca1. 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.
source: http://www.pnas.org/...4/8375.abstract
Suppression of Nerve Growth Factor Trk Receptors and Prolactin Receptors by Endocannabinoids Leads to Inhibition of Human Breast and Prostate Cancer Cell Proliferation1
Dominique Melck, Luciano De Petrocellis, Pierangelo Orlando, Tiziana Bisogno, Chiara Laezza, Maurizio Bifulco and Vincenzo Di Marzo
Istituto per la Chimica di Molecole di Interesse Biologico (D.M., T.B., V.D.M.), Istituto di Cibernetica (L.D.P.), and Istituto di Biochimica delle Proteine ed Enzimologia (P.O.), Consiglio Nazionale delle Ricerche, 80072 Arco Felice (NA); and Centro di Endocrinologia e Oncologia Sperimentale, Consiglio Nazionale delle Ricerche, and Dipartimento di Biologia e Patologia Cellulare e Molecolare, Universit di Napoli Federico II (C.L., M.B.), 80131 Naples, Italy
Address all correspondence and requests for reprints to: Dr. Vincenzo Di Marzo, Istituto per la Chimica di Molecole di Interesse Biologico, Consiglio Nazionale delle Ricerche, 80072 Arco Felice (NA), Italy. E-mail: vdm@trinc.icmib.na.cnr.it.
Anandamide and 2-arachidonoylglycerol (2-AG), two endogenous ligands of the CB1 and CB2 cannabinoid receptor subtypes, inhibit the proliferation of PRL-responsive human breast cancer cells (HBCCs) through down-regulation of the long form of the PRL receptor (PRLr). Here we report that 1) anandamide and 2-AG inhibit the nerve growth factor (NGF)-induced proliferation of HBCCs through suppression of the levels of NGF Trk receptors; 2) inhibition of PRLr levels results in inhibition of the proliferation of other PRL-responsive cells, the prostate cancer DU-145 cell line; and 3) CB1-like cannabinoid receptors are expressed in HBCCs and DU-145 cells and mediate the inhibition of cell proliferation and Trk/PRLr exp<b></b>ression. -NGF-induced HBCC proliferation was potently inhibited (IC50 = 50600 nM) by the synthetic cannabinoid HU-210, 2-AG, anandamide, and its metabolically stable analogs, but not by the anandamide congener, palmitoylethanolamide, or the selective agonist of CB2 cannabinoid receptors, BML-190. The effect of anandamide was blocked by the CB1 receptor antagonist, SR141716A, but not by the CB2 receptor antagonist, SR144528. Anandamide and HU-210 exerted a strong inhibition of the levels of NGF Trk receptors as detected by Western immunoblotting; this effect was reversed by SR141716A. When induced by exogenous PRL, the proliferation of prostate DU-145 cells was potently inhibited (IC50 = 100300 nM) by anandamide, 2-AG, and HU-210. Anandamide also down-regulated the levels of PRLr in DU-145 cells. SR141716A attenuated these two effects of anandamide. HBCCs and DU-145 cells were shown to contain 1) transcripts for CB1 and, to a lesser extent, CB2 cannabinoid receptors, 2) specific binding sites for [3H]SR141716A that could be displaced by anandamide, and 3) a CB1 receptor-immunoreactive protein. These findings suggest that endogenous cannabinoids and CB1 receptor agonists are potential negative effectors of PRL- and NGF-induced biological responses, at least in some cancer cells.
source: http://endo.endojour...tract/141/1/118
CHEMOTHERAPY, ANTIBIOTICS, AND GENE THERAPY
Antitumor Activity of Plant Cannabinoids with Emphasis on the Effect of Cannabidiol on Human Breast Carcinoma
Alessia Ligresti, Aniello Schiano Moriello, Katarzyna Starowicz, Isabel Matias, Simona Pisanti, Luciano De Petrocellis, Chiara Laezza, Giuseppe Portella, Maurizio Bifulco, and Vincenzo Di Marzo
Endocannabinoid Research Group, Istituto di Chimica Biomolecolare (A.L., A.S.M., K.S., I.M., V.D.M.), and Istituto di Cibernetica (A.S.M., L.D.P.), Consiglio Nazionale delle Ricerche Pozzuoli, Italy; Dipartimento di Biologia e Patologia Cellulare e Molecolare "L. Califano", Universit di Napoli "Federico II", Napoli, Italy (S.P., C.L., G.P., M.B.); and Dipartimento di Scienze Farmaceutiche, Universit degli Studi di Salerno, Fisciano, Italy (S.P., M.B.)
9-Tetrahydrocannabinol (THC) exhibits antitumor effects on various cancer cell types, but its use in chemotherapy is limited by its psychotropic activity. We investigated the antitumor activities of other plant cannabinoids, i.e., cannabidiol, cannabigerol, cannabichromene, cannabidiol acid and THC acid, and assessed whether there is any advantage in using Cannabis extracts (enriched in either cannabidiol or THC) over pure cannabinoids. Results obtained in a panel of tumor cell lines clearly indicate that, of the five natural compounds tested, cannabidiol is the most potent inhibitor of cancer cell growth (IC50 between 6.0 and 10.6 M), with significantly lower potency in noncancer cells. The cannabidiol-rich extract was equipotent to cannabidiol, whereas cannabigerol and cannabichromene followed in the rank of potency. Both cannabidiol and the cannabidiol-rich extract inhibited the growth of xenograft tumors obtained by s.c. injection into athymic mice of human MDA-MB-231 breast carcinoma or rat v-K-ras-transformed thyroid epithelial cells and reduced lung metastases deriving from intrapaw injection of MDA-MB-231 cells. Judging from several experiments on its possible cellular and molecular mechanisms of action, we propose that cannabidiol lacks a unique mode of action in the cell lines investigated. At least for MDA-MB-231 cells, however, our experiments indicate that cannabidiol effect is due to its capability of inducing apoptosis via: direct or indirect activation of cannabinoid CB2 and vanilloid transient receptor potential vanilloid type-1 receptors and cannabinoid/vanilloid receptor-independent elevation of intracellular Ca2+ and reactive oxygen species. Our data support the further testing of cannabidiol and cannabidiol-rich extracts for the potential treatment of cancer
source: http://jpet.aspetjou...ract/318/3/1375
9-Tetrahydrocannabinol Inhibits Cell Cycle Progression in Human Breast Cancer Cells through Cdc2 Regulation
Mara M. Caffarel1, David Sarri2, Jos Palacios2, Manuel Guzmn1 and Cristina Snchez1
1 Department of Biochemistry and Molecular Biology I, School of Biology, Complutense University and 2 Breast and Gynecological Cancer Group, Molecular Pathology Programme, Centro Nacional de Investigaciones Oncolgicas, Madrid, Spain
Requests for reprints: Cristina Snchez, Department of Biochemistry and Molecular Biology I, School of Biology, Complutense University, 28040 Madrid, Spain. Phone: 34-913944668; Fax: 34-913944672; E-mail: csg@bbm1.ucm.es.
It has been proposed that cannabinoids are involved in the control of cell fate. Thus, these compounds can modulate proliferation, differentiation, and survival in different manners depending on the cell type and its physiopathologic context. However, little is known about the effect of cannabinoids on the cell cycle, the main process controlling cell fate. Here, we show that 9-tetrahydrocannabinol (THC), through activation of CB2 cannabinoid receptors, reduces human breast cancer cell proliferation by blocking the progression of the cell cycle and by inducing apoptosis. In particular, THC arrests cells in G2-M via down-regulation of Cdc2, as suggested by the decreased sensitivity to THC acquired by Cdc2-overexpressing cells. Of interest, the proliferation pattern of normal human mammary epithelial cells was much less affected by THC. We also analyzed by real-time quantitative PCR the exp<b></b>ression of CB1 and CB2 cannabinoid receptors in a series of human breast tumor and nontumor samples. We found a correlation between CB2 exp<b></b>ression and histologic grade of the tumors. There was also an association between CB2 exp<b></b>ression and other markers of prognostic and predictive value, such as estrogen receptor, progesterone receptor, and ERBB2/HER-2 oncogene. Importantly, no significant CB2 exp<b></b>ression was detected in nontumor breast tissue. Taken together, these data might set the bases for a cannabinoid therapy for the management of breast cancer.(Cancer Res 2006; 66(13): 6615-21)
source: http://cancerres.aac...ract/66/13/6615
Science: A combination of THC and prochlorperazine effective in reducing nausea and vomiting in women following breast surgery
Researchers of the University of Arkansas and the Central Arkansas Veterans Hospital System investigated the effects of 5 mg oral THC and 25 mg rectal prochlorperazine on the rate of nausea and vomiting in women following breast surgery under general anaesthesia. The rate of nausea decreased from 59 per cent to 15 per cent and the rate of vomiting from 29 per cent to 3 per cent compared to non-treated patients.
A retrospective review of 242 eligible patients, who underwent surgery between July 2001 and March 2003 was performed. 127 patients received surgery before September 2002 and did not receive a prophylaxis. 115 patients received surgery after September 2002 and were treated before surgery with oral THC (dronabinol) and rectal prochlorperazine. Data were collected from hospital records. Researchers concluded that post-operative nausea and vomiting (PONV) is a "significant problem in breast surgical patients. Preoperative treatment with dronabinol and prochlorperazine significantly reduced the number and severity of episodes of PONV."
source: http://www.cannabis-...el.php?id=219#1
Science: Cannabidiol inhibits tumour growth in leukaemia and breast cancer in animal studies
Italian researchers investigated the anti-tumour effects of five natural cannabinoids of the cannabis plant (cannabidiol, cannabigerol, cannabichromene, cannabidiol-acid and THC-acid) in breast cancer. Cannabidiol (CBD) was the most potent cannabinoid in inhibiting the growth of human breast cancer cells that had been injected under the skin of mice. CBD also reduced lung metastases deriving from human breast cancer cells that had been injected into the paws of the animals.
Researchers found that the anti-tumour effects of CBD were caused by induction of apoptosis (programmed cell death). They concluded that their data "support the further testing of cannabidiol and cannabidiol-rich extracts for the potential treatment of cancer."
These observations are supported by investigations of US scientists who found out that exposure of leukaemia cells to CBD led to a reduction in cell viability and induction of apoptosis. In living animals CBD caused a reduction in number of leukaemia cells. The scientists noted that CBD "may be a novel and highly selective treatment for leukemia."
source: http://www.cannabis-...el.php?id=220#2
Science: A combination of THC and prochlorperazine effective in reducing nausea and vomiting in women following breast surgery
Researchers of the University of Arkansas and the Central Arkansas Veterans Hospital System investigated the effects of 5 mg oral THC and 25 mg rectal prochlorperazine on the rate of nausea and vomiting in women following breast surgery under general anaesthesia. The rate of nausea decreased from 59 per cent to 15 per cent and the rate of vomiting from 29 per cent to 3 per cent compared to non-treated patients.
A retrospective review of 242 eligible patients, who underwent surgery between July 2001 and March 2003 was performed. 127 patients received surgery before September 2002 and did not receive a prophylaxis. 115 patients received surgery after September 2002 and were treated before surgery with oral THC (dronabinol) and rectal prochlorperazine. Data were collected from hospital records. Researchers concluded that post-operative nausea and vomiting (PONV) is a "significant problem in breast surgical patients. Preoperative treatment with dronabinol and prochlorperazine significantly reduced the number and severity of episodes of PONV."
source: http://www.cannabis-...el.php?id=219#1
Medical Marijuana Takes On New Meaning for Metastatic Breast Cancer
If you have breast cancer, you may have considered the use of medical marijuana at some point during your chemo treatment. Smoking marijuana has provided some women with relief from the nausea and vomiting that can accompany chemo, relief that the range of normal side effect drugs werent able to give. Some states permit the legal use of medical marijuana; most dont. Nevertheless, most women who want to try marijuana seem to be able to get it. Personally, I didnt experience any severe problems with nausea. But I was astounded at the number of people who, prior to treatment, offered to get me a supply if I thought I needed it!
Now, doctors at the California Pacific Medical Center Research Institute in San Francisco have released a study, in the current issue of Molecular Cancer Therapeutics, that may in the future open the door to a much more critical use of marijuana: stopping the spread of metastatic breast cancer. It seems that a compound found in cannabis (the scientific name for marijuana), CBD, has been shown (in the lab) to stop the human gene Id-1 from directing cancer cells to multiply and spread.
California Pacific Senior researcher Pierre-Yves Desprez, in an interview with HealthDay News, noted that the Id-1 genes are very bad. They push the cells to behave like embryonic cells and grow. They go crazy, they proliferate, they migrate. We need to be able to turn them off."
Desprez and fellow researcher Sean D. McAllister joined forces just two years ago. Desprez had been studying the Id-1 gene for 12 years; McAllister was a cannabis expert, but not involved in cancer research. Together they found that Id-1 is the orchestra conductor that directs breast cancer cells to grow and spread. And that CBD inhibits Id-1; it turns it off, puts it to sleep, pick your metaphor. Bottom line, it neutralizes it. And the cancer stops spreading.
Both researchers pointed out that CBD is non-toxic and non-psychoactive. In other words, patients wouldnt get high taking it. And its non-toxicity is an important attribute; Desprez and McAllister predict that, to be effective, patients might have to take CBD for several years. They also cautioned that smoking marijuana isnt going to cure metastatic breast cancer; the level of CBD necessary to inhibit Id-1 simply cant be obtained that way.
While studies are still very much in the preliminary stages, its interesting to think that a plant that has been used medicinally for nearly 5,000 years may in the future be a key element in controlling cancer. As recently as 1937 (when it was outlawed in the U.S.), marijuana (cannabis sativa) was being touted as an analgesic, anti-emetic, narcotic, and sedative.
Parke-Davis, once Americas oldest and largest drug manufacturer (and now a division of drug giant Pfizer), offered Fluid Extract Cannabis via catalogs. Until the invention of aspirin in the mid-1800s, cannabis was the civilized worlds main pain reliever. Now its illegal. Heres hoping that someday soon cannabis returns, this time as a successful treatment for metastatic breast cancer.
source: http://www.healthcen...6/takes-cancer/
Marijuana Compound May Stop Breast Cancer From Spreading, Study Says
A compound found in cannabis may stop breast cancer from spreading throughout the body, according to a new study by scientists at California Pacific Medical Center Research Institute. The researchers are hopeful that the compound called CBD, which is found in cannabis sativa, could be a non-toxic alternative to chemotherapy.
"Right now we have a limited range of options in treating aggressive forms of cancer," said lead researcher Dr. Sean D. McAllister, a cancer researcher at CPMCRI, in a news release. "Those treatments, such as chemotherapy, can be effective but they can also be extremely toxic and difficult for patients. This compound offers the hope of a non-toxic therapy that could achieve the same results without any of the painful side effects."
The researchers tested CBD to inhibit the activity of a gene called Id-1, which is believed to be responsible for the aggressive spread of cancer cells throughout the body, away from the original tumor site.
"We know that Id-1 is a key regulator of the spread of breast cancer," said Dr. Pierre-Yves Desprez, a cancer researcher at CPMCRI and the senior author of the study, in a news release. "We also know that Id-1 has also been found at higher levels in other forms of cancer. So what is exciting about this study is that if CBD can inhibit Id-1 in breast cancer cells, then it may also prove effective at stopping the spread of cancer cells in other forms of the disease, such as colon and brain or prostate cancer."
Comparing it with another ingredient isolated from marijuana called THC, which is used in some medical treatments, the researchers said CBD does not have any psychoactive properties, so using it would not violate any state or federal laws. However, the researchers stressed that they are not suggesting that breast cancer patients smoke marijuana. They say it is highly unlikely that effective concentrations of CBD could be reached by smoking pot.
The study is published in the latest issue of the journal Molecular Cancer Therapeutics.
source: http://www.foxnews.c...,312132,00.html
Sean D. McAllister, PhD
Introduction
Our research team is studying the potential of the endocannabinoid system to control cell fate with the goal of developing therapeutic interventions for aggressive cancers. This newly discovered biological system can be regulated by many different classes of cannabinoid compounds that work through specific cellular receptors. The cloned cannabinoid receptors have been termed cannabinoid 1 (CB1) and (CB2).
9-tetrahydrocannabinol (THC), a mixed CB1 and CB2 receptor agonist, is the primary active constituent of Cannabis sativa and is currently being used in a clinical trial for the treatment of aggressive recurrent glioblastoma multiforme (GBM). Cannabinoids are also being used in clinical trials for purposes unrelated to their direct anticancer activity. The compounds have been reported to be well tolerated during chronic oral and systemic administration. In addition to 9-THC, cannabidiol (CBD), cannabinol (CBN) and cannabigerol (CBG) are also present in reasonable quantities in Cannabis. CBN has low affinity for CB1 and CB2 receptors, whereas the non-psychotropic cannabinoids, CBD and CBG, have negligible affinity for the cloned receptors. We have determined that these additional cannabinoids are also effective and inhibiting aggressive cancers. Importantly, we have discovered in vitro that a synergistic increase in the antiproliferative and apoptotic activity of cannabinoids can be produced by combining specific ratios of CB1 and CB2 receptors agonists with non-psychotropic cannabinoids.
We are currently determining the molecular mechanism that may explain the synergistic increase in anticancer activity that is observed with the combination treatments. We are also studying whether this combination strategy will lead to greater antitumor activity in vivo.
In addition to the combination therapy project, we are working in collaboration with Dr. Pierre Desprez to develop novel inhibitors of Id-1 using cannabinoid compounds. Id-1 is a helix-loop-helix protein that acts as an inhibitor of basic helix-loop-helix transcription factors that control cell differentiation, development and carcinogenesis. Past research of Id-1 exp<b></b>ression in normal and cancerous breast cells, as well as in mouse mammary glands and in human breast cancer biopsies, demonstrated that increased Id-1 exp<b></b>ression was associated with a proliferative and invasive phenotype. Specifically, it was found that Id-1 was constitutively expressed at a high level in aggressive breast cancer cells and human biopsies, and that aggressiveness was reverted in vitro and in vivo when Id-1 exp<b></b>ression was targeted using antisense technology. Importantly, we have recently discovered that CBD, a nontoxic cannabinoid that lacks psychoactivity, can inhibit Id-1 gene exp<b></b>ression in metastatic breast cancer cells and consequently their aggressive phenotype. The down-regulation of exp<b></b>ression was the result of the inhibition of the endogenous Id-1 promoter and corresponding mRNA and protein levels. CBD and compounds based off of its structure can therefore potentially be used as therapeutic agents. CBD also inhibits breast cancer metastasis in vivo.
Based off of our recent findings, we are currently involved in 1) developing novel CBD analogs for the treat of aggressive breast cancers 2) discovering the detailed mechanisms through which cannabinoid compounds regulate Id-1 exp<b></b>ression.
source: http://www.cpmc.org/...ience/sean.html
McAllister SD, Christian RT, Horowitz MP, Garcia A, Desprez PY.
California Pacific Medical Center, Research Institute, 475 Brannan Street, San Francisco, CA 94107, USA. mcallis@cpmcri.org
Invasion and metastasis of aggressive breast cancer cells is the final and fatal step during cancer progression, and is the least understood genetically. Clinically, there are still limited therapeutic interventions for aggressive and metastatic breast cancers available. Clearly, effective and nontoxic therapies are urgently required. Id-1, an inhibitor of basic helix-loop-helix transcription factors, has recently been shown to be a key regulator of the metastatic potential of breast and additional cancers. Using a mouse model, we previously determined that metastatic breast cancer cells became significantly less invasive in vitro and less metastatic in vivo when Id-1 was down-regulated by stable transduction with antisense Id-1. It is not possible at this point, however, to use antisense technology to reduce Id-1 exp<b></b>ression in patients with metastatic breast cancer. Here, we report that cannabidiol (CBD), a cannabinoid with a low-toxicity profile, could down-regulate Id-1 exp<b></b>ression in aggressive human breast cancer cells. The CBD concentrations effective at inhibiting Id-1 exp<b></b>ression correlated with those used to inhibit the proliferative and invasive phenotype of breast cancer cells. CBD was able to inhibit Id-1 exp<b></b>ression at the mRNA and protein level in a concentration-dependent fashion. These effects seemed to occur as the result of an inhibition of the Id-1 gene at the promoter level. Importantly, CBD did not inhibit invasiveness in cells that ectopically expressed Id-1. In conclusion, CBD represents the first nontoxic exogenous agent that can significantly decrease Id-1 exp<b></b>ression in metastatic breast cancer cells leading to the down-regulation of tumor aggressiveness.
source: http://www.ncbi.nlm....Pubmed_RVDocSum
N. California Researchers Testing Whether Marijuana Chemical Can Slow Cancer Growth, With Funding by Susan G. Komen for the Cure
Largest Breast Cancer Organization Investing $60 Million to Research Despite Down Economy
SAN FRANCISCO, April 9 /PRNewswire-USNewswire/ -- Testing whether a powerful ingredient in marijuana can help slow the growth of aggressive breast cancer cells is just one of six Bay Area breast cancer studies being funded this year by Susan G. Komen for the Cure, the global leader in the breast cancer movement announced today.
The projects are part of a $60 million portfolio of 2009 research grants that Komen for the Cure is investing with scientists worldwide to find the cures for breast cancer.
"Breast cancer doesn't care about the economy, and with more than 1.3 million new cases of breast cancer expected this year, the need for new research is more urgent than ever," said Hala Moddelmog, Komen's CEO and president.
In the Bay Area this year, Komen's $1.8 million in grants will go to the University of California at San Francisco, Stanford University School of Medicine and California Pacific Medical Center.
<strong>The UCSF study will try to improve bilingual communication and education between Latinas and their health care providers. One Stanford grant, if successful, could reverse some of the debilitating neurological and cognitive side effects of brain metastases, halt the progression of disease and possibly reduce mortality. And CPMC researchers will test whether cannabidiol - an ingredient in marijuana - can inhibit the aggressive growth of some breast cancers.</strong>
"Komen's infusion of millions of dollars into research projects means that promising research that is designed to treat and ultimately eradicate breast cancer will continue," said Eric Winer, M.D., Komen's chief scientific advisor.
During the past 27 years, Komen has invested $400 million to fund research globally, starting with Komen's first grant in 1982 for $28,000. A decade later, the annual total had grown to 21 grants worth $590,000 and 10 years after that, Komen distributed $21 million in research funds. This year, Komen is providing researchers worldwide with $60 million. In the last three years alone, Komen has invested nearly $237 million for breast cancer research.
In 2008, Komen created Promise Grants - a new category of multi-year, multi-million dollar grants designed to discover and deliver cures for breast cancer more quickly.
Here is a list of local institutions, the researchers and the projects Komen is funding this year, pending agreements:
University of California at San Francisco
*Celia Kaplan, $450,185, Breast Cancer Risk Reduction in Primary Care Clinics: A Bilingual Intervention for Women and Physicians
Stanford University School of Medicine
*Irene Wapnir, $600,000, From Bench to Bedside: Treatment of Breast Cancer Brain Metastasis with 131I and Radiosensitizers
*Roeland Nusse, $180,000, 'Wnt signaling in human breast cancer stem cells.
*Michael Clarke, $180,000, Functions of microRNAs in metastatic tumor initiating cells of human breast cancer
*Howard Chang, $180,000, Noncoding RNA, Polycomb and Breast Cancer Progression
California Pacific Medical Center
*Sean McAlister, $593,713, Inhibition of Breast Cancer Cell Aggressiveness by Cannabidiol
About Susan G. Komen for the Cure
Nancy G. Brinker promised her dying sister, Susan G. Komen, she would do everything in her power to end breast cancer forever. In 1982, that promise became Susan G. Komen for the Cure and launched the global breast cancer movement. Today, Komen for the Cure is the world's largest grassroots network of breast cancer survivors and activists fighting to save lives, empower people, ensure quality care for all and energize science to find the cures. Thanks to events like the Komen Race for the Cure, we have invested more than $1.3 billion to fulfill our promise, becoming the largest source of nonprofit funds dedicated to the fight against breast cancer in the world. For more information about Susan G. Komen for the Cure, breast health or breast cancer, visit www.komen.org or call 1-877 GO KOMEN.
SOURCE Susan G. Komen for the Cure
source: http://news.prnewswi...C...3872&EDATE=
Cannabis compound 'halts cancer'
The CBD compound found in cannabis is non-toxicA compound found in cannabis may stop breast cancer spreading throughout the body, US scientists believe.The California Pacific Medical Center Research Institute team are hopeful that cannabidiol or CBD could be a non-toxic alternative to chemotherapy.
Unlike cannabis, CBD does not have any psychoactive properties so its use would not violate laws, Molecular Cancer Therapeutics reports.
The authors stressed that they were not suggesting patients smoke marijuana.
They added that it would be highly unlikely that effective concentrations of CBD could be reached by smoking cannabis.
This compound offers the hope of a non-toxic therapy that could achieve the same results without any of the painful side effects <br clear="all">
Lead researcher Dr Sean McAllister
CBD works by blocking the activity of a gene called Id-1 which is believed to be responsible for the aggressive spread of cancer cells away from the original tumour site - a process called metastasis.
Past work has shown CBD can block aggressive human brain cancers.
The latest work found CBD appeared to have a similar effect on breast cancer cells in the lab.
Future hope
Lead researcher Dr Sean McAllister said: "Right now we have a limited range of options in treating aggressive forms of cancer.
"Those treatments, such as chemotherapy, can be effective but they can also be extremely toxic and difficult for patients.
"This compound offers the hope of a non-toxic therapy that could achieve the same results without any of the painful side effects."
Dr Joanna Owens of Cancer Research UK said: "This research is at a very early stage.
"The findings will need to be followed up with clinical trials in humans to see if the CBD is safe, and whether the beneficial effects can be replicated.
"Several cancer drugs based on plant chemicals are already used widely, such as vincristine - which is derived from a type of flower called Madagascar Periwinkle and is used to treat breast and lung cancer. It will be interesting to see whether CBD will join them."
Maria Leadbeater of Breast Cancer Care said: "Many people experience side-effects while having chemotherapy, such as nausea and an increased risk of infection, which can take both a physical and emotional toll.
"Any drug that has fewer side-effects will, of course, be of great interest."
But she added: "It is clear that much more research needs to be carried out."
Caution content may be shocking!
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![[Image: Everything%2BYou%2BNeed%2Bto%2BKnow%2BAb...252529.jpg]](http://3.bp.blogspot.com/-RJS7VVNUWMQ/TgmFGpIFJyI/AAAAAAAACGg/hBnmun_ub4w/s1600/Everything%2BYou%2BNeed%2Bto%2BKnow%2BAbout%2BBreast%2BCancer%2B%2525285%252529.jpg)
WHAT IS BREAST CANCER?
Breast cancer itself is a malignant tumor than can form in one or both breasts, and usually develops in the milk-producing ducts of the breast, known as the the lobules. According to the website www.Cancer.org:
Breast cancer is the most common cancer among women in the United States, other than skin cancer. It is the second leading cause of cancer death in women, after lung cancer. The chance of a woman having invasive breast cancer some time during her life is a little less 1 in 8. The chance of dying from breast cancer is about 1 in 35.
Now Breast Cancer isn't only found in women, it can also occur in men, although not as common, but just as deadly.
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The most recent statistics for 2011 from the American Cancer Society estimate as follows:
HOW CAN YOU PREVENT IT?
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THE GENETIC FACTORSBecause there is a higher chance of cancer in women with a family history, women should consult a medical professional who is specifically trained in risk assessment in order to help you decide the best methods for early detection. In Western countries, up to 10% of breast cancer is attributed to genetic predisposition. It can be transmitted through either the mother or father, with the possibility of either parent transmitting the abnormality without ever developing it -- as in, they're simply carriers.
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However, an excess of ovarian, colon, prostatic, and other cancers are inherited in the same abnormal mutation as breast cancer, so if any of these are present in family members, it is recommended that you take precautions. Most breast cancers are due to genetic mutations, with women who get the disease at an early age predisposed to the development of breast cancer.
Mentioned on www.MindFully.org:
WHERE IN THE WORLD IS CANCER?
Saturday, November 24 2007 @ 12:31 AM EST
Edited by: Michael Hess
Cannabidiol may be helpful in reducing the aggressiveness of breast cancer cells
BBSNews 2007-11-24 -- (IACM) In a mouse model of metastatic breast cancer the natural non- psychotropic cannabinoid cannabidiol (CBD) reduced the aggressiveness of breast cancer cells.
CBD inhibited a protein called Id-1. Id proteins play an important role in tumour cell biology. The researchers of the California Pacific Medical Center Research Institute concluded that "CBD represents the first nontoxic exogenous agent that can significantly decrease Id- 1 exp<b></b>ression in metastatic breast cancer cells leading to the down-regulation of tumor aggressiveness."
The authors stressed that they were not suggesting patients smoke cannabis. They added that it would be highly unlikely that effective concentrations of CBD could be reached by smoking cannabis. Lead researcher Dr. Sean McAllister said: "Right now we have a limited range of options in treating aggressive forms of cancer. Those treatments, such as chemotherapy, can be effective but they can also be extremely toxic and difficult for patients. This compound offers the hope of a non-toxic therapy that could achieve the same results without any of the painful side effects."
(Sources: BBC News of 19 November 2007; McAllister SD, Christian RT, Horowitz MP, Garcia A, Desprez PY. Cannabidiol as a novel inhibitor of Id-1 gene exp<b></b>ression in aggressive breast cancer cells. Mol Cancer Ther 2007;6(11):2921-7.)
source: http://bbsnews.net/a...071124003153693
The endogenous cannabinoid anandamide inhibits human breast cancer cell proliferation
Luciano De Petrocellis*,, Dominique Melck*,, Antonella Palmisano, Tiziana Bisogno, Chiara Laezza, Maurizio Bifulco, and Vincenzo Di Marzo,
+Author Affiliations
Istituto di Cibernetica and Istituto per la Chimica di Molecole di Interesse Biologico (affiliated with the National Institute for the Chemistry of Biological Systems, Consiglio Nazionale delle Ricerche), Consiglio Nazionale delle Ricerche, Via Toiano 6, 80072 Arco Felice, Naples, Italy; Istituto di Ricerche sullAdattamento dei Bovini e dei Bufali allAmbiente del Mezzogiorno, Consiglio Nazionale delle Ricerche, Ponticelli, 80147 Naples, Italy; and Centro di Studio der lEndocrinologia e lOncologia Sperimentale, Consiglio Nazionale Delle Richerche and Dipartimento di Biologia e Patologia Cellulare e Molecolare, Universit di Napoli Federico II, 80131 Naples, Italy
Communicated by Rita Levi-Montalcini, Institute of Neurobiology, Consiglio Nazionale delle Ricerche, Rome, Italy (received for review March 6, 1998)
Abstract
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 M and 8392% maximal inhibition at 510 M. The proliferation of several other nonmammary tumoral cell lines was not affected by 10 M 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. A stable analogue of anandamide -methanandamide, another endogenous cannabinoid, 2-arachidonoylglycerol, and the synthetic cannabinoid HU-210 also inhibited EFM-19 cell proliferation, whereas arachidonic acid was much less effective. These cannabimimetic substances displaced the binding of the selective cannabinoid agonist [3H]CP 55,940 to EFM-19 membranes with an order of potency identical to that observed for the inhibition of EFM-19 cell proliferation. Moreover, anandamide cytostatic effect was inhibited by the selective CB1 receptor antagonist SR 141716A. Cell proliferation was arrested by a prolactin mAb and enhanced by exogenous human prolactin, whose mitogenic action was reverted by very low (0.10.5 M) doses of anandamide. Anandamide suppressed the levels of the long form of the prolactin receptor in both EFM-19 and MCF-7 cells, as well as a typical prolactin-induced response, i.e., the exp<b></b>ression of the breast cancer cell susceptibility gene brca1. 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.
source: http://www.pnas.org/...4/8375.abstract
Suppression of Nerve Growth Factor Trk Receptors and Prolactin Receptors by Endocannabinoids Leads to Inhibition of Human Breast and Prostate Cancer Cell Proliferation1
Dominique Melck, Luciano De Petrocellis, Pierangelo Orlando, Tiziana Bisogno, Chiara Laezza, Maurizio Bifulco and Vincenzo Di Marzo
Istituto per la Chimica di Molecole di Interesse Biologico (D.M., T.B., V.D.M.), Istituto di Cibernetica (L.D.P.), and Istituto di Biochimica delle Proteine ed Enzimologia (P.O.), Consiglio Nazionale delle Ricerche, 80072 Arco Felice (NA); and Centro di Endocrinologia e Oncologia Sperimentale, Consiglio Nazionale delle Ricerche, and Dipartimento di Biologia e Patologia Cellulare e Molecolare, Universit di Napoli Federico II (C.L., M.B.), 80131 Naples, Italy
Address all correspondence and requests for reprints to: Dr. Vincenzo Di Marzo, Istituto per la Chimica di Molecole di Interesse Biologico, Consiglio Nazionale delle Ricerche, 80072 Arco Felice (NA), Italy. E-mail: vdm@trinc.icmib.na.cnr.it.
Anandamide and 2-arachidonoylglycerol (2-AG), two endogenous ligands of the CB1 and CB2 cannabinoid receptor subtypes, inhibit the proliferation of PRL-responsive human breast cancer cells (HBCCs) through down-regulation of the long form of the PRL receptor (PRLr). Here we report that 1) anandamide and 2-AG inhibit the nerve growth factor (NGF)-induced proliferation of HBCCs through suppression of the levels of NGF Trk receptors; 2) inhibition of PRLr levels results in inhibition of the proliferation of other PRL-responsive cells, the prostate cancer DU-145 cell line; and 3) CB1-like cannabinoid receptors are expressed in HBCCs and DU-145 cells and mediate the inhibition of cell proliferation and Trk/PRLr exp<b></b>ression. -NGF-induced HBCC proliferation was potently inhibited (IC50 = 50600 nM) by the synthetic cannabinoid HU-210, 2-AG, anandamide, and its metabolically stable analogs, but not by the anandamide congener, palmitoylethanolamide, or the selective agonist of CB2 cannabinoid receptors, BML-190. The effect of anandamide was blocked by the CB1 receptor antagonist, SR141716A, but not by the CB2 receptor antagonist, SR144528. Anandamide and HU-210 exerted a strong inhibition of the levels of NGF Trk receptors as detected by Western immunoblotting; this effect was reversed by SR141716A. When induced by exogenous PRL, the proliferation of prostate DU-145 cells was potently inhibited (IC50 = 100300 nM) by anandamide, 2-AG, and HU-210. Anandamide also down-regulated the levels of PRLr in DU-145 cells. SR141716A attenuated these two effects of anandamide. HBCCs and DU-145 cells were shown to contain 1) transcripts for CB1 and, to a lesser extent, CB2 cannabinoid receptors, 2) specific binding sites for [3H]SR141716A that could be displaced by anandamide, and 3) a CB1 receptor-immunoreactive protein. These findings suggest that endogenous cannabinoids and CB1 receptor agonists are potential negative effectors of PRL- and NGF-induced biological responses, at least in some cancer cells.
source: http://endo.endojour...tract/141/1/118
CHEMOTHERAPY, ANTIBIOTICS, AND GENE THERAPY
Antitumor Activity of Plant Cannabinoids with Emphasis on the Effect of Cannabidiol on Human Breast Carcinoma
Alessia Ligresti, Aniello Schiano Moriello, Katarzyna Starowicz, Isabel Matias, Simona Pisanti, Luciano De Petrocellis, Chiara Laezza, Giuseppe Portella, Maurizio Bifulco, and Vincenzo Di Marzo
Endocannabinoid Research Group, Istituto di Chimica Biomolecolare (A.L., A.S.M., K.S., I.M., V.D.M.), and Istituto di Cibernetica (A.S.M., L.D.P.), Consiglio Nazionale delle Ricerche Pozzuoli, Italy; Dipartimento di Biologia e Patologia Cellulare e Molecolare "L. Califano", Universit di Napoli "Federico II", Napoli, Italy (S.P., C.L., G.P., M.B.); and Dipartimento di Scienze Farmaceutiche, Universit degli Studi di Salerno, Fisciano, Italy (S.P., M.B.)
9-Tetrahydrocannabinol (THC) exhibits antitumor effects on various cancer cell types, but its use in chemotherapy is limited by its psychotropic activity. We investigated the antitumor activities of other plant cannabinoids, i.e., cannabidiol, cannabigerol, cannabichromene, cannabidiol acid and THC acid, and assessed whether there is any advantage in using Cannabis extracts (enriched in either cannabidiol or THC) over pure cannabinoids. Results obtained in a panel of tumor cell lines clearly indicate that, of the five natural compounds tested, cannabidiol is the most potent inhibitor of cancer cell growth (IC50 between 6.0 and 10.6 M), with significantly lower potency in noncancer cells. The cannabidiol-rich extract was equipotent to cannabidiol, whereas cannabigerol and cannabichromene followed in the rank of potency. Both cannabidiol and the cannabidiol-rich extract inhibited the growth of xenograft tumors obtained by s.c. injection into athymic mice of human MDA-MB-231 breast carcinoma or rat v-K-ras-transformed thyroid epithelial cells and reduced lung metastases deriving from intrapaw injection of MDA-MB-231 cells. Judging from several experiments on its possible cellular and molecular mechanisms of action, we propose that cannabidiol lacks a unique mode of action in the cell lines investigated. At least for MDA-MB-231 cells, however, our experiments indicate that cannabidiol effect is due to its capability of inducing apoptosis via: direct or indirect activation of cannabinoid CB2 and vanilloid transient receptor potential vanilloid type-1 receptors and cannabinoid/vanilloid receptor-independent elevation of intracellular Ca2+ and reactive oxygen species. Our data support the further testing of cannabidiol and cannabidiol-rich extracts for the potential treatment of cancer
source: http://jpet.aspetjou...ract/318/3/1375
9-Tetrahydrocannabinol Inhibits Cell Cycle Progression in Human Breast Cancer Cells through Cdc2 Regulation
Mara M. Caffarel1, David Sarri2, Jos Palacios2, Manuel Guzmn1 and Cristina Snchez1
1 Department of Biochemistry and Molecular Biology I, School of Biology, Complutense University and 2 Breast and Gynecological Cancer Group, Molecular Pathology Programme, Centro Nacional de Investigaciones Oncolgicas, Madrid, Spain
Requests for reprints: Cristina Snchez, Department of Biochemistry and Molecular Biology I, School of Biology, Complutense University, 28040 Madrid, Spain. Phone: 34-913944668; Fax: 34-913944672; E-mail: csg@bbm1.ucm.es.
It has been proposed that cannabinoids are involved in the control of cell fate. Thus, these compounds can modulate proliferation, differentiation, and survival in different manners depending on the cell type and its physiopathologic context. However, little is known about the effect of cannabinoids on the cell cycle, the main process controlling cell fate. Here, we show that 9-tetrahydrocannabinol (THC), through activation of CB2 cannabinoid receptors, reduces human breast cancer cell proliferation by blocking the progression of the cell cycle and by inducing apoptosis. In particular, THC arrests cells in G2-M via down-regulation of Cdc2, as suggested by the decreased sensitivity to THC acquired by Cdc2-overexpressing cells. Of interest, the proliferation pattern of normal human mammary epithelial cells was much less affected by THC. We also analyzed by real-time quantitative PCR the exp<b></b>ression of CB1 and CB2 cannabinoid receptors in a series of human breast tumor and nontumor samples. We found a correlation between CB2 exp<b></b>ression and histologic grade of the tumors. There was also an association between CB2 exp<b></b>ression and other markers of prognostic and predictive value, such as estrogen receptor, progesterone receptor, and ERBB2/HER-2 oncogene. Importantly, no significant CB2 exp<b></b>ression was detected in nontumor breast tissue. Taken together, these data might set the bases for a cannabinoid therapy for the management of breast cancer.(Cancer Res 2006; 66(13): 6615-21)
source: http://cancerres.aac...ract/66/13/6615
Science: A combination of THC and prochlorperazine effective in reducing nausea and vomiting in women following breast surgery
Researchers of the University of Arkansas and the Central Arkansas Veterans Hospital System investigated the effects of 5 mg oral THC and 25 mg rectal prochlorperazine on the rate of nausea and vomiting in women following breast surgery under general anaesthesia. The rate of nausea decreased from 59 per cent to 15 per cent and the rate of vomiting from 29 per cent to 3 per cent compared to non-treated patients.
A retrospective review of 242 eligible patients, who underwent surgery between July 2001 and March 2003 was performed. 127 patients received surgery before September 2002 and did not receive a prophylaxis. 115 patients received surgery after September 2002 and were treated before surgery with oral THC (dronabinol) and rectal prochlorperazine. Data were collected from hospital records. Researchers concluded that post-operative nausea and vomiting (PONV) is a "significant problem in breast surgical patients. Preoperative treatment with dronabinol and prochlorperazine significantly reduced the number and severity of episodes of PONV."
source: http://www.cannabis-...el.php?id=219#1
Science: Cannabidiol inhibits tumour growth in leukaemia and breast cancer in animal studies
Italian researchers investigated the anti-tumour effects of five natural cannabinoids of the cannabis plant (cannabidiol, cannabigerol, cannabichromene, cannabidiol-acid and THC-acid) in breast cancer. Cannabidiol (CBD) was the most potent cannabinoid in inhibiting the growth of human breast cancer cells that had been injected under the skin of mice. CBD also reduced lung metastases deriving from human breast cancer cells that had been injected into the paws of the animals.
Researchers found that the anti-tumour effects of CBD were caused by induction of apoptosis (programmed cell death). They concluded that their data "support the further testing of cannabidiol and cannabidiol-rich extracts for the potential treatment of cancer."
These observations are supported by investigations of US scientists who found out that exposure of leukaemia cells to CBD led to a reduction in cell viability and induction of apoptosis. In living animals CBD caused a reduction in number of leukaemia cells. The scientists noted that CBD "may be a novel and highly selective treatment for leukemia."
source: http://www.cannabis-...el.php?id=220#2
Science: A combination of THC and prochlorperazine effective in reducing nausea and vomiting in women following breast surgery
Researchers of the University of Arkansas and the Central Arkansas Veterans Hospital System investigated the effects of 5 mg oral THC and 25 mg rectal prochlorperazine on the rate of nausea and vomiting in women following breast surgery under general anaesthesia. The rate of nausea decreased from 59 per cent to 15 per cent and the rate of vomiting from 29 per cent to 3 per cent compared to non-treated patients.
A retrospective review of 242 eligible patients, who underwent surgery between July 2001 and March 2003 was performed. 127 patients received surgery before September 2002 and did not receive a prophylaxis. 115 patients received surgery after September 2002 and were treated before surgery with oral THC (dronabinol) and rectal prochlorperazine. Data were collected from hospital records. Researchers concluded that post-operative nausea and vomiting (PONV) is a "significant problem in breast surgical patients. Preoperative treatment with dronabinol and prochlorperazine significantly reduced the number and severity of episodes of PONV."
source: http://www.cannabis-...el.php?id=219#1
Medical Marijuana Takes On New Meaning for Metastatic Breast Cancer
If you have breast cancer, you may have considered the use of medical marijuana at some point during your chemo treatment. Smoking marijuana has provided some women with relief from the nausea and vomiting that can accompany chemo, relief that the range of normal side effect drugs werent able to give. Some states permit the legal use of medical marijuana; most dont. Nevertheless, most women who want to try marijuana seem to be able to get it. Personally, I didnt experience any severe problems with nausea. But I was astounded at the number of people who, prior to treatment, offered to get me a supply if I thought I needed it!
Now, doctors at the California Pacific Medical Center Research Institute in San Francisco have released a study, in the current issue of Molecular Cancer Therapeutics, that may in the future open the door to a much more critical use of marijuana: stopping the spread of metastatic breast cancer. It seems that a compound found in cannabis (the scientific name for marijuana), CBD, has been shown (in the lab) to stop the human gene Id-1 from directing cancer cells to multiply and spread.
California Pacific Senior researcher Pierre-Yves Desprez, in an interview with HealthDay News, noted that the Id-1 genes are very bad. They push the cells to behave like embryonic cells and grow. They go crazy, they proliferate, they migrate. We need to be able to turn them off."
Desprez and fellow researcher Sean D. McAllister joined forces just two years ago. Desprez had been studying the Id-1 gene for 12 years; McAllister was a cannabis expert, but not involved in cancer research. Together they found that Id-1 is the orchestra conductor that directs breast cancer cells to grow and spread. And that CBD inhibits Id-1; it turns it off, puts it to sleep, pick your metaphor. Bottom line, it neutralizes it. And the cancer stops spreading.
Both researchers pointed out that CBD is non-toxic and non-psychoactive. In other words, patients wouldnt get high taking it. And its non-toxicity is an important attribute; Desprez and McAllister predict that, to be effective, patients might have to take CBD for several years. They also cautioned that smoking marijuana isnt going to cure metastatic breast cancer; the level of CBD necessary to inhibit Id-1 simply cant be obtained that way.
While studies are still very much in the preliminary stages, its interesting to think that a plant that has been used medicinally for nearly 5,000 years may in the future be a key element in controlling cancer. As recently as 1937 (when it was outlawed in the U.S.), marijuana (cannabis sativa) was being touted as an analgesic, anti-emetic, narcotic, and sedative.
Parke-Davis, once Americas oldest and largest drug manufacturer (and now a division of drug giant Pfizer), offered Fluid Extract Cannabis via catalogs. Until the invention of aspirin in the mid-1800s, cannabis was the civilized worlds main pain reliever. Now its illegal. Heres hoping that someday soon cannabis returns, this time as a successful treatment for metastatic breast cancer.
source: http://www.healthcen...6/takes-cancer/
Marijuana Compound May Stop Breast Cancer From Spreading, Study Says
A compound found in cannabis may stop breast cancer from spreading throughout the body, according to a new study by scientists at California Pacific Medical Center Research Institute. The researchers are hopeful that the compound called CBD, which is found in cannabis sativa, could be a non-toxic alternative to chemotherapy.
"Right now we have a limited range of options in treating aggressive forms of cancer," said lead researcher Dr. Sean D. McAllister, a cancer researcher at CPMCRI, in a news release. "Those treatments, such as chemotherapy, can be effective but they can also be extremely toxic and difficult for patients. This compound offers the hope of a non-toxic therapy that could achieve the same results without any of the painful side effects."
The researchers tested CBD to inhibit the activity of a gene called Id-1, which is believed to be responsible for the aggressive spread of cancer cells throughout the body, away from the original tumor site.
"We know that Id-1 is a key regulator of the spread of breast cancer," said Dr. Pierre-Yves Desprez, a cancer researcher at CPMCRI and the senior author of the study, in a news release. "We also know that Id-1 has also been found at higher levels in other forms of cancer. So what is exciting about this study is that if CBD can inhibit Id-1 in breast cancer cells, then it may also prove effective at stopping the spread of cancer cells in other forms of the disease, such as colon and brain or prostate cancer."
Comparing it with another ingredient isolated from marijuana called THC, which is used in some medical treatments, the researchers said CBD does not have any psychoactive properties, so using it would not violate any state or federal laws. However, the researchers stressed that they are not suggesting that breast cancer patients smoke marijuana. They say it is highly unlikely that effective concentrations of CBD could be reached by smoking pot.
The study is published in the latest issue of the journal Molecular Cancer Therapeutics.
source: http://www.foxnews.c...,312132,00.html
Sean D. McAllister, PhD
Introduction
Our research team is studying the potential of the endocannabinoid system to control cell fate with the goal of developing therapeutic interventions for aggressive cancers. This newly discovered biological system can be regulated by many different classes of cannabinoid compounds that work through specific cellular receptors. The cloned cannabinoid receptors have been termed cannabinoid 1 (CB1) and (CB2).
9-tetrahydrocannabinol (THC), a mixed CB1 and CB2 receptor agonist, is the primary active constituent of Cannabis sativa and is currently being used in a clinical trial for the treatment of aggressive recurrent glioblastoma multiforme (GBM). Cannabinoids are also being used in clinical trials for purposes unrelated to their direct anticancer activity. The compounds have been reported to be well tolerated during chronic oral and systemic administration. In addition to 9-THC, cannabidiol (CBD), cannabinol (CBN) and cannabigerol (CBG) are also present in reasonable quantities in Cannabis. CBN has low affinity for CB1 and CB2 receptors, whereas the non-psychotropic cannabinoids, CBD and CBG, have negligible affinity for the cloned receptors. We have determined that these additional cannabinoids are also effective and inhibiting aggressive cancers. Importantly, we have discovered in vitro that a synergistic increase in the antiproliferative and apoptotic activity of cannabinoids can be produced by combining specific ratios of CB1 and CB2 receptors agonists with non-psychotropic cannabinoids.
We are currently determining the molecular mechanism that may explain the synergistic increase in anticancer activity that is observed with the combination treatments. We are also studying whether this combination strategy will lead to greater antitumor activity in vivo.
In addition to the combination therapy project, we are working in collaboration with Dr. Pierre Desprez to develop novel inhibitors of Id-1 using cannabinoid compounds. Id-1 is a helix-loop-helix protein that acts as an inhibitor of basic helix-loop-helix transcription factors that control cell differentiation, development and carcinogenesis. Past research of Id-1 exp<b></b>ression in normal and cancerous breast cells, as well as in mouse mammary glands and in human breast cancer biopsies, demonstrated that increased Id-1 exp<b></b>ression was associated with a proliferative and invasive phenotype. Specifically, it was found that Id-1 was constitutively expressed at a high level in aggressive breast cancer cells and human biopsies, and that aggressiveness was reverted in vitro and in vivo when Id-1 exp<b></b>ression was targeted using antisense technology. Importantly, we have recently discovered that CBD, a nontoxic cannabinoid that lacks psychoactivity, can inhibit Id-1 gene exp<b></b>ression in metastatic breast cancer cells and consequently their aggressive phenotype. The down-regulation of exp<b></b>ression was the result of the inhibition of the endogenous Id-1 promoter and corresponding mRNA and protein levels. CBD and compounds based off of its structure can therefore potentially be used as therapeutic agents. CBD also inhibits breast cancer metastasis in vivo.
Based off of our recent findings, we are currently involved in 1) developing novel CBD analogs for the treat of aggressive breast cancers 2) discovering the detailed mechanisms through which cannabinoid compounds regulate Id-1 exp<b></b>ression.
source: http://www.cpmc.org/...ience/sean.html
McAllister SD, Christian RT, Horowitz MP, Garcia A, Desprez PY.
California Pacific Medical Center, Research Institute, 475 Brannan Street, San Francisco, CA 94107, USA. mcallis@cpmcri.org
Invasion and metastasis of aggressive breast cancer cells is the final and fatal step during cancer progression, and is the least understood genetically. Clinically, there are still limited therapeutic interventions for aggressive and metastatic breast cancers available. Clearly, effective and nontoxic therapies are urgently required. Id-1, an inhibitor of basic helix-loop-helix transcription factors, has recently been shown to be a key regulator of the metastatic potential of breast and additional cancers. Using a mouse model, we previously determined that metastatic breast cancer cells became significantly less invasive in vitro and less metastatic in vivo when Id-1 was down-regulated by stable transduction with antisense Id-1. It is not possible at this point, however, to use antisense technology to reduce Id-1 exp<b></b>ression in patients with metastatic breast cancer. Here, we report that cannabidiol (CBD), a cannabinoid with a low-toxicity profile, could down-regulate Id-1 exp<b></b>ression in aggressive human breast cancer cells. The CBD concentrations effective at inhibiting Id-1 exp<b></b>ression correlated with those used to inhibit the proliferative and invasive phenotype of breast cancer cells. CBD was able to inhibit Id-1 exp<b></b>ression at the mRNA and protein level in a concentration-dependent fashion. These effects seemed to occur as the result of an inhibition of the Id-1 gene at the promoter level. Importantly, CBD did not inhibit invasiveness in cells that ectopically expressed Id-1. In conclusion, CBD represents the first nontoxic exogenous agent that can significantly decrease Id-1 exp<b></b>ression in metastatic breast cancer cells leading to the down-regulation of tumor aggressiveness.
source: http://www.ncbi.nlm....Pubmed_RVDocSum
N. California Researchers Testing Whether Marijuana Chemical Can Slow Cancer Growth, With Funding by Susan G. Komen for the Cure
Largest Breast Cancer Organization Investing $60 Million to Research Despite Down Economy
SAN FRANCISCO, April 9 /PRNewswire-USNewswire/ -- Testing whether a powerful ingredient in marijuana can help slow the growth of aggressive breast cancer cells is just one of six Bay Area breast cancer studies being funded this year by Susan G. Komen for the Cure, the global leader in the breast cancer movement announced today.
The projects are part of a $60 million portfolio of 2009 research grants that Komen for the Cure is investing with scientists worldwide to find the cures for breast cancer.
"Breast cancer doesn't care about the economy, and with more than 1.3 million new cases of breast cancer expected this year, the need for new research is more urgent than ever," said Hala Moddelmog, Komen's CEO and president.
In the Bay Area this year, Komen's $1.8 million in grants will go to the University of California at San Francisco, Stanford University School of Medicine and California Pacific Medical Center.
<strong>The UCSF study will try to improve bilingual communication and education between Latinas and their health care providers. One Stanford grant, if successful, could reverse some of the debilitating neurological and cognitive side effects of brain metastases, halt the progression of disease and possibly reduce mortality. And CPMC researchers will test whether cannabidiol - an ingredient in marijuana - can inhibit the aggressive growth of some breast cancers.</strong>
"Komen's infusion of millions of dollars into research projects means that promising research that is designed to treat and ultimately eradicate breast cancer will continue," said Eric Winer, M.D., Komen's chief scientific advisor.
During the past 27 years, Komen has invested $400 million to fund research globally, starting with Komen's first grant in 1982 for $28,000. A decade later, the annual total had grown to 21 grants worth $590,000 and 10 years after that, Komen distributed $21 million in research funds. This year, Komen is providing researchers worldwide with $60 million. In the last three years alone, Komen has invested nearly $237 million for breast cancer research.
In 2008, Komen created Promise Grants - a new category of multi-year, multi-million dollar grants designed to discover and deliver cures for breast cancer more quickly.
Here is a list of local institutions, the researchers and the projects Komen is funding this year, pending agreements:
University of California at San Francisco
*Celia Kaplan, $450,185, Breast Cancer Risk Reduction in Primary Care Clinics: A Bilingual Intervention for Women and Physicians
Stanford University School of Medicine
*Irene Wapnir, $600,000, From Bench to Bedside: Treatment of Breast Cancer Brain Metastasis with 131I and Radiosensitizers
*Roeland Nusse, $180,000, 'Wnt signaling in human breast cancer stem cells.
*Michael Clarke, $180,000, Functions of microRNAs in metastatic tumor initiating cells of human breast cancer
*Howard Chang, $180,000, Noncoding RNA, Polycomb and Breast Cancer Progression
California Pacific Medical Center
*Sean McAlister, $593,713, Inhibition of Breast Cancer Cell Aggressiveness by Cannabidiol
About Susan G. Komen for the Cure
Nancy G. Brinker promised her dying sister, Susan G. Komen, she would do everything in her power to end breast cancer forever. In 1982, that promise became Susan G. Komen for the Cure and launched the global breast cancer movement. Today, Komen for the Cure is the world's largest grassroots network of breast cancer survivors and activists fighting to save lives, empower people, ensure quality care for all and energize science to find the cures. Thanks to events like the Komen Race for the Cure, we have invested more than $1.3 billion to fulfill our promise, becoming the largest source of nonprofit funds dedicated to the fight against breast cancer in the world. For more information about Susan G. Komen for the Cure, breast health or breast cancer, visit www.komen.org or call 1-877 GO KOMEN.
SOURCE Susan G. Komen for the Cure
source: http://news.prnewswi...C...3872&EDATE=
Cannabis compound 'halts cancer'
The CBD compound found in cannabis is non-toxicA compound found in cannabis may stop breast cancer spreading throughout the body, US scientists believe.The California Pacific Medical Center Research Institute team are hopeful that cannabidiol or CBD could be a non-toxic alternative to chemotherapy.
Unlike cannabis, CBD does not have any psychoactive properties so its use would not violate laws, Molecular Cancer Therapeutics reports.
The authors stressed that they were not suggesting patients smoke marijuana.
They added that it would be highly unlikely that effective concentrations of CBD could be reached by smoking cannabis.
This compound offers the hope of a non-toxic therapy that could achieve the same results without any of the painful side effects <br clear="all">
Lead researcher Dr Sean McAllister
CBD works by blocking the activity of a gene called Id-1 which is believed to be responsible for the aggressive spread of cancer cells away from the original tumour site - a process called metastasis.
Past work has shown CBD can block aggressive human brain cancers.
The latest work found CBD appeared to have a similar effect on breast cancer cells in the lab.
Future hope
Lead researcher Dr Sean McAllister said: "Right now we have a limited range of options in treating aggressive forms of cancer.
"Those treatments, such as chemotherapy, can be effective but they can also be extremely toxic and difficult for patients.
"This compound offers the hope of a non-toxic therapy that could achieve the same results without any of the painful side effects."
Dr Joanna Owens of Cancer Research UK said: "This research is at a very early stage.
"The findings will need to be followed up with clinical trials in humans to see if the CBD is safe, and whether the beneficial effects can be replicated.
"Several cancer drugs based on plant chemicals are already used widely, such as vincristine - which is derived from a type of flower called Madagascar Periwinkle and is used to treat breast and lung cancer. It will be interesting to see whether CBD will join them."
Maria Leadbeater of Breast Cancer Care said: "Many people experience side-effects while having chemotherapy, such as nausea and an increased risk of infection, which can take both a physical and emotional toll.
"Any drug that has fewer side-effects will, of course, be of great interest."
But she added: "It is clear that much more research needs to be carried out."
Caution content may be shocking!
WHAT IS BREAST CANCER?
Breast cancer itself is a malignant tumor than can form in one or both breasts, and usually develops in the milk-producing ducts of the breast, known as the the lobules. According to the website www.Cancer.org:
Breast cancer is the most common cancer among women in the United States, other than skin cancer. It is the second leading cause of cancer death in women, after lung cancer. The chance of a woman having invasive breast cancer some time during her life is a little less 1 in 8. The chance of dying from breast cancer is about 1 in 35.
Now Breast Cancer isn't only found in women, it can also occur in men, although not as common, but just as deadly.
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The most recent statistics for 2011 from the American Cancer Society estimate as follows:
- About 230,480 new cases of invasive breast cancer in women
- About 57,650 new cases of carcinoma in situ (CIS) will be found (CIS is non-invasive and is the earliest form of breast cancer).
- About 39,520 deaths from breast cancer (women)
HOW CAN YOU PREVENT IT?
THE GENETIC FACTORSBecause there is a higher chance of cancer in women with a family history, women should consult a medical professional who is specifically trained in risk assessment in order to help you decide the best methods for early detection. In Western countries, up to 10% of breast cancer is attributed to genetic predisposition. It can be transmitted through either the mother or father, with the possibility of either parent transmitting the abnormality without ever developing it -- as in, they're simply carriers.
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However, an excess of ovarian, colon, prostatic, and other cancers are inherited in the same abnormal mutation as breast cancer, so if any of these are present in family members, it is recommended that you take precautions. Most breast cancers are due to genetic mutations, with women who get the disease at an early age predisposed to the development of breast cancer.Mentioned on www.MindFully.org:
WHERE IN THE WORLD IS CANCER?
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