Give Me Medical Marijuana, or Give Me Death!
An Open Letter to Rhode Island Governor Lincoln Chafee
Image: Photograph by loranger, CC BY 2.0 License
Info: Lincoln Chafee Website
Dear Governor Chafee,
I have recently heard that you shut down Medical Marijuana Centers, on the grounds that "Unfortunately, Rhode Island's compassion center law is illegal under paramount federal law." (TokeOfTheTown.com) This is from your official comments in rejecting the right of patients to seek appropriate medicine for their conditions. Many of these patients are going to be terminally-ill patients now, because of your decision. That is to say, they are guaranteed to die from their disease, but only when the government steps in and directly prohibits them from receiving their medicine. You ought to be more concerned without violating the right to life and liberty, guaranteed by the US Constitution and by federal law, than with opposing the federal government's unconstitutional demands.
Allow me to provide you with some articles showing that the federal government DOES provide marijuana to patients who have sued, on the grounds that without it, their quality of life would be unbearable. Published by Boston.com, "US gives marijuana to a select few patients." (Articles.Boston.com) And, published by CarmiTimes, "Federal government gives away 'pot.'" (Carmitimes.com) Now, the federal government is providing marijuana to patients who absolutely need this, and they're providing it free of charge. But you made the decision to shut down compassion centers that help these people, because it violates "federal law."
Are you aware that Biological and Chemical Warfare is prohibited by the US government and by numerous international treaties? Here's a follow-up question: Do you know how Chemotherapy, the current medicine used to "treat" cancer, is made? It's made from Mustine (Mechlorethamine), a byproduct of Mustard Gas -- that is to say, a first-class, well-known chemical weapon. It is prohibited by US law, international law, etc., etc.. Have you shut down any hospitals that puts Mustard Gas into the veins of their cancer patients? You seem to be so anxious to follow orders that trickle down the chain of command from the top, to be obedient to what the federal government asks but not what it is obligated to do. Shut down hospitals that make millions for biomedical corporations because they're filling patients with Mustard gas? Absolutely not! Let's shut down Medical Marijuana clinics -- what a brilliant idea.
Can Marijuana treat cancer? Yes. A federal government report in 1974 declares as much: "Marijuana cures cancer – US government has known since 1974." (Patients4MedicalMarijuana.Wordpress.com) The Federal Government has passed a law, providing finances for cancer research, and that research verifies that Marijuana is perhaps the only known cure for it? So then what are you, and what have you done, as a governor, while SIXTY MILLION AMERICANS died from cancer since the cure was discovered? In one study by Harvard University, lung-cancer is cut in half by the use of Marijuana. (ScienceDaily.com) Here's another report, all the way back from 2004, Alternet.org.
First, it seems quite clear that Marijuana cures cancer, and that the federal government knows this quite well, with any of its statements otherwise simply being what a prosecuting attorney would call, "Willful Negligence." (If you don't know anything about the use of Marijuana to cure cancer, you should be the last human being on the planet to step in the way of those who do.) Second, according to some federal laws, the constitution, and local state laws, it's clear that murder is prohibited. Third, these people who are dying because of your decisions are not dying because of a disease -- that would be amazingly convenient for everyone in power. That's like saying people who die from machine-gun fire from police are dying from the physics of projectile-motion. The truth is, they're dying because someone ordered it. Someone in power screamed to those below them to tear up and rip apart some poor, powerless group.
"Beitfel ist Beitfel!" That was the defense of the Nazis at the Nuremberg trials. "Orders are orders, the law is the law, I'm not concerned with who dies, how many die, or what comes from it, because of the law. I just follow it." With sixty million dead already under your state's programs, this comparison is completely justified.
But isn't murder illegal? I used to think so, until I watched how my government behaves. If murder was illegal, you would be arresting federal troops for interfering with local Cannabis production. Why? Even the federal government gives away medical marijuana for free, because it is the only thing that can save the lives of those sick from cancer. If you want to stop murder, you'd have your local police tailing the DEA agencies, you'd be working to protect marijuana users from these unconstitutional laws, and you'd be doing something more than condemning sick patients to death.
And yet you're the government!!! According to your past record, you've never done anything to stop murder and death. You thrive off of it. All you would have to do to cure these awful diseases is to provide Medical Marijuana to all cancer patients. But that's the problem. That's like saying all you would have to do to cure an infection in the Middle Ages is apply rubbing alcohol. But they would burn you alive as a heretic for talking about something so unusual as "the Germ Theory of Disease." And nothing has changed today, except you burn people alive for Political Superstitions instead of Religious Superstitions. People are dying from cancer? No, nobody is dying from cancer. They're being killed by their government, in a sort of ritualistic-style murder you'd only find from the macabre stories of witch-burnings.
"The best kings desire to be in a position to be wicked, if they please, without forfeiting their mastery: political sermonisers may tell them to their hearts' content that, the people's strength being their own, their first interest is that the people should be prosperous, numerous and formidable; they are well aware that this is untrue. Their first personal interest is that the people should be weak, wretched, and unable to resist them."
--Jean Jacques Rousseau, 1762
"The Social Contract"
Image: Photograph by Graffiti Land, CC BY-NC 2.0 License
Attached is a list of resources on Marijuana's ability to treat Cancer...
"Antineoplastic activity of cannabinoids." 1975 Sep - Journal of the National Cancer Institute. By A.E. Munson, L.S. Harris, M.A. Friedman, W.L. Dewey, and R.A. Carchman. Erowid.org.
"Lewis lung adenocarcinoma growth was retarded by the oral administration of delta-9-tetrahydrocannabinol, delta-8-tetrahydrocannabinol, and cannabinol (CBN), but not cannabidiol (CBD). Animals treated for 10 consecutive days with delta-9-THC, beginning the day after tumor implantation, demonstrated a dose-dependent action of retarded tumor growth. Mice treated for 20 consecutive days with delta-8-THC and CBN had reduced primary tumor size. CBD showed no inhibitory effect on tumor growth at 14, 21, or 28 days. Delta-9-THC, delta-8-THC, and CBN increased the mean survival time (36% at 100 mg/kg, 25% at 200 mg/kg, and 27% at 50 mg/kg;, respectively), whereas CBD did not. Delta-9-THC administered orally daily until death in doses of 50, 100, or 200 mg/kg did not increase the life-spans of (C57BL/6 X DBA/2) F (BDF) mice hosting the L1210 murine leukemia. However, delta-9-THC administered daily for 10 days significantly inhibited Friend leukemia virus-induced splenomegaly by 71% at 200 mg/kg..."
"Marijuana use and cancer incidence (California, United States)." 1997 Sep 8 - Cancer Causes Control Journal. By Sidney S, Quesenberry CP Jr, Friedman GD, and Tekawa IS. NCBI.NLM.NIH.gov.
"Marijuana use also was not associated with tobacco-related cancers or with cancer of the following sites: colorectal, lung, melanoma, prostate, breast, cervix. Among nonsmokers of tobacco cigarettes, ever having used marijuana was associated with increased risk of prostate cancer (RR = 3.1, CI = 1.0-9.5) and nearly significantly increased risk of cervical cancer (RR = 1.4, CI = 1.0-2.1). We conclude that, in this relatively young study cohort, marijuana use and cancer were not associated in overall analyses..."
"Induction and regulation of the carcinogen-metabolizing enzyme CYP1A1 by marijuana smoke and delta (9)-tetrahydrocannabinol." 2001 Mar - American Journal of Cell and Molecular Biology. By Roth MD, Marques-Magallanes JA, Yuan M, Sun W, Tashkin DP, Hankinson O. NCBI.NLM.NIH.gov.
"Induction of the carcinogen-metabolizing enzyme cytochrome P4501A1 (CYP1A1) is a key step in the development of tobacco-related cancers. To determine if marijuana smoke activates CYP1A1, a murine hepatoma cell line expressing an inducible CYP1A1 gene (Hepa-1) was exposed in vitro to tar extracts prepared from either tobacco, marijuana, or placebo marijuana cigarettes. Marijuana tar induced higher levels of CYP1A1 messenger RNA (mRNA) than did tobacco tar, yet resulted in much lower CYP1A1 enzyme activity."
"Marijuana smoking and head and neck cancer." 2002 Nov 1 - Journal of Clinical Pharmacology. By M Hashibe, DE Ford, and ZF Zhang. JCP.SagePub.com.
"However, in a cohort study with 8 years of follow-up, marijuana use was not associated with increased risks of all cancers or smoking-related cancers. Further epidemiological studies are necessary to confirm the association of marijuana smoking with head and neck cancers and to examine marijuana smoking as a risk factor for lung cancer."
"Inhibition of skin tumor growth and angiogenesis in vivo by activation of cannabinoid receptors." 2003 Jan 1 - Journal of Clinical Investigation. By M. Llanos Casanova, Cristina Blázquez, Jesús Martínez-Palacio, Concepción Villanueva, M. Jesús Fernández-Aceñero, John W. Huffman, José L. Jorcano and Manuel Guzmán. JCI.org.
"Cannabinoids inhibit skin tumor growth in vivo. Given the inhibition of tumorigenic epidermal cell survival in culture by cannabinoids, we evaluated the effect of cannabinoid treatment on skin tumor growth in vivo. Tumors generated by inoculation of the highly malignant PDV.C57 cell line were treated with vehicle or WIN-55,212-2. As shown in Figure 5, a–c, cannabinoid administration blocked the growth of tumor cells in vivo (in 75% of the mice treated)....
"Cannabinoids inhibit skin tumor angiogenesis in vivo. Tumors require an adequate supply of oxygen and nutrients to grow more than a few millimeters. For that purpose they produce proangiogenic factors that promote the formation of new blood vessels (28, 29). We therefore analyzed whether the vascularization of growth-arrested cannabinoid-treated tumors was affected. Northern blot analyses showed that the expression of major proangiogenic factors, namely VEGF, PIGF, and Ang2, was strongly depressed by treatment with WIN-55,212-2 or JWH-133 (Figure 6a). The mRNA expression of Ang1 and the two antiangiogenic factors, thrombospondin 1 and thrombospondin 2, was not significantly affected by cannabinoid administration (data not shown). Furthermore, although immunostaining of CD31, a marker of endothelial cells, revealed no significant differences in vascular density (number of blood vessels per unit area) between control and WIN-55,212-2– or JWH-133–treated tumors (Figures 6, b and c), important differences were observed when vessel morphology was examined: while control carcinomas showed a network of dilated vessels, cannabinoid-treated tumors displayed a pattern of blood vessels characterized predominantly by narrow capillaries (Figure 6b). Morphometric analyses confirmed that cannabinoid treatment induced a statistically significant decrease in blood vessel size, as determined by the total area occupied by vessels, the area per vessel, and the vessel larger diameter length (Figure 6c)."
"Inhibition of tumor angiogenesis by cannabinoids." 2003 Jan 2 - The Journal of the Federation of American Scientists for Experimental Biology. By Cristina Blázquez, M. Llanos Casanova, Anna Planas, Teresa Gómez Del Pulgar, Concepción Villanueva, María J. Fernández-Aceñero, Julián Aragonés, John W. Huffman, José L. Jorcano And Manuel Guzmán. Fasebj.org.
"We found that tumors from cannabinoid-treated animals were smaller and paler than controls (Fig. 1 A, B). Analysis of the vasculature by immunostaining of CD31, an endothelial cell marker, revealed no significant effect of JWH-133 on microvascular count (number of blood vessels per unit area) in the tumors (data not shown). However, cannabinoid administration turned the microvascular hyperplasia of control tumors (Fig. 1C, E ) to a pattern of blood vessels characterized predominantly by very small and narrow capillaries (Fig. 1D, F ). Moreover, whereas control tumors showed a fractionated immunostaining of smooth muscle ?-actin (SMA) (Fig. 1G ), a smooth muscle cell and pericyte marker, in cannabinoid-treated tumors SMA-positive cells had a mature appearance and remained closely investing the endothelial wall (Fig. 1H )."
"Antitumor Effects of Cannabidiol, a Nonpsychoactive Cannabinoid, on Human Glioma Cell Lines." 2003 Nov 14 - The Journal of Pharmacology and Experimental Therapeutics. By Paola Massi, Angelo Vaccani, Stefania Ceruti, Arianna Colombo, Maria P. Abbracchio, and Daniela Parolaro. JPET.AspetJournals.org.
"In the current study we demonstrated that the nonpsychoactive cannabinoid compound CBD can induce in vitro and in vivo inhibition of tumoral cell growth, and we also showed, for the first time, that CBD can trigger the apoptosis of human gliomas, a very aggressive tumor characterized by poor clinical prognosis and unsatisfactory response to the currently available pharmacological agents."
"Cannabinoids and ceramide: two lipids acting hand-by-hand." 2005 Aug 19 - Life Sciences Journal. By Velasco G, Galve-Roperh I, Sánchez C, Blázquez C, Haro A, Guzmán M. NCBI.NLM.NIH.gov.
"Cannabinoids, the active components of Cannabis sativa (marijuana) and their endogenous counterparts, exert their effects by binding to specific G-protein-coupled receptors that modulate adenylyl cyclase and ion channels. Recent research has shown that the CB1 cannabinoid receptor is also coupled to the generation of the lipid second messenger ceramide via two different pathways: sphingomyelin hydrolysis and ceramide synthesis de novo. Sustained ceramide accumulation in tumor cells mediates cannabinoid-induced apoptosis, as evidenced by in vitro and in vivo studies. This effect seems to be due to the impact of ceramide on key cell signalling systems such as the extracellular signal-regulated kinase cascade and the Akt pathway. These findings provide a new conceptual view on how cannabinoids act, and raise interesting physiological and therapeutic questions."
"Cannabinoids selectively inhibit proliferation and induce death of cultured human glioblastoma multiforme cells." 2005 - Journal of Neuro-Oncology. By Sean D. Mc Allister, Calvin Chan, Ryan J. Taft, Tri Luu, Mary E. Abood, Dan H. Moore, Ken Aldape and Garret Yount. SpringerLink.com.
"We evaluated the influence of cannabinoids on cell proliferation, death, and morphology of human GBM cell lines and in primary human glial cultures, the normal cells from which GBM tumors arise. The influence of a plant derived cannabinoid agonist, delta9-tetrahydrocannabinol delta9-THC), and a potent synthetic cannabinoid agonist, WIN 55,212-2, were compared using time lapse microscopy. We discovered that delta9-THC decreases cell proliferation and increases cell death of human GBM cells more rapidly than WIN 55,212-2. delta9-THC was also more potent at inhibiting the proliferation of GBM cells compared to WIN 55,212-2. The effects of delta9-THC and WIN 55,212-2 on the GBM cells were partially the result of cannabinoid receptor activation. The same concentration of delta9-THC that significantly inhibits proliferation and increases death of human GBM cells has no significant impact on human primary glial cultures."
"Antitumor Activity of Plant Cannabinoids with Emphasis on the Effect of Cannabidiol on Human Breast Carcinoma." 2006 Sep - The Journal of Pharmacology and Experimental Therapeutics. By Alessia Ligresti, Aniello Schiano Moriello, Katarzyna Starowicz, Isabel Matias, Simona Pisanti, Luciano De Petrocellis, Chiara Laezza, Giuseppe Portella, Maurizio Bifulco and Vincenzo Di Marzo. Jpet.AspetJournals.org
"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."
"Marijuana Use and the Risk of Lung and Upper Aerodigestive Tract Cancers: Results of a Population-Based Case-Control Study." 2006 Oct 15 - American Association for Cancer Research Journal. By Mia Hashibe, Hal Morgenstern, Yan Cui, Donald P. Tashkin, Zuo-Feng Zhang, Wendy Cozen, Thomas M. Mack, and Sander Greenland. CEBP.AACRJournals.org.
"Despite several lines of evidence suggesting the biological plausibility of marijuana being carcinogenic, epidemiologic findings are inconsistent. We conducted a population-based case-control study of the association between marijuana use and the risk of lung and upper aerodigestive tract cancers in Los Angeles....
"Our results may have been affected by selection bias or error in measuring lifetime exposure and confounder histories; but they suggest that the association of these cancers with marijuana, even long-term or heavy use, is not strong and may be below practically detectable limits."
"Delta9-Tetrahydrocannabinol inhibits epithelial growth factor-induced lung cancer cell migration in vitro as well as its growth and metastasis in vivo." 2007 Jul 9 - Epub. By Preet A, Ganju RK, and Groopman JE. NCBI.NLM.NIH.gov.
"In this study, we characterized the effects of THC on the EGF-induced growth and metastasis of human non-small cell lung cancer using the cell lines A549 and SW-1573 as in vitro models. We found that these cells express the cannabinoid receptors CB(1) and CB(2), known targets for THC action, and that THC inhibited EGF-induced growth, chemotaxis and chemoinvasion. Moreover, signaling studies indicated that THC may act by inhibiting the EGF-induced phosphorylation of ERK1/2, JNK1/2 and AKT. THC also induced the phosphorylation of focal adhesion kinase at tyrosine 397. Additionally, in in vivo studies in severe combined immunodeficient mice, there was significant inhibition of the subcutaneous tumor growth and lung metastasis of A549 cells in THC-treated animals as compared to vehicle-treated controls."
"Cannabidiol as a novel inhibitor of Id-1 gene expression in aggressive breast cancer cells." 2007 Nov - Molecular Cancer Therapeutics. By Sean D. McAllister, Rigel T. Christian, Maxx P. Horowitz, Amaia Garcia and, Pierre-Yves Desprez. MCT.ACCRJournals.org.
"...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 expression in patients with metastatic breast cancer. Here, we report that cannabidiol (CBD), a cannabinoid with a low-toxicity profile, could down-regulate Id-1 expression in aggressive human breast cancer cells. The CBD concentrations effective at inhibiting Id-1 expression correlated with those used to inhibit the proliferative and invasive phenotype of breast cancer cells. CBD was able to inhibit Id-1 expression 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 expression in metastatic breast cancer cells leading to the down-regulation of tumor aggressiveness."
"Inhibition of Cancer Cell Invasion by Cannabinoids via Increased Expression of Tissue Inhibitor of Matrix Metalloproteinases-1." 2007 Dec 25 - Journal of the National Cancer Institute. By Robert Ramer and Burkhard Hinz. JNCI.OxfordJournals.org.
"In conclusion, our results suggest that there exists a signaling pathway by which the binding of cannabinoids to specifi c receptors leads via intracellular MAPK activation to induction of TIMP-1 expression and subsequent inhibition of tumor cell invasion. To our knowledge, this is the fi rst report of TIMP-1 – dependent antiinvasive effects of cannabinoids. This signaling pathway may play an important role in the antimetastatic action of cannabinoids, whose potential therapeutic benefi t in the treatment of highly invasive cancers should be addressed in clinical trials."
"Cannabinoids for Cancer Treatment: Progress and Promise." 2008 Jan 15 - Cancer Research Journal. By Sami Sarfaraz, Vaqar M. Adhami, Deeba N. Syed, Farrukh Afaq, and Hasan Mukhtar. Cancerres.AACRJournals.org.
"Cannabinoids are a class of pharmacologic compounds that offer potential applications as antitumor drugs, based on the ability of some members of this class to limit inflammation, cell proliferation, and cell survival. In particular, emerging evidence suggests that agonists of cannabinoid receptors expressed by tumor cells may offer a novel strategy to treat cancer."
"Cannabis use and cancer of the head and neck: case-control study." 2008 Mar - Otolaryngology -- Head and Neck Surgery. By Aldington S, Harwood M, Cox B, Weatherall M, Beckert L, Hansell A, Pritchard A, Robinson G, Beasley R; Cannabis and Respiratory Disease Research Group. NCBI.NLM.NIH.gov.
"There were 75 cases and 319 controls. An increased risk of cancer was found with increasing tobacco use, alcohol consumption, and decreased income but not increasing cannabis use."
"Loss of cannabinoid receptor 1 accelerates intestinal tumor growth." 2008 Aug 1 - Cancer Research Journal. By Dingzhi Wang, Haibin Wang, Wei Ning, Michael G. Backlund, Sudhansu K. Dey, and Raymond N. DuBois. NCBI.NLM.NIH.gov.
"In conclusion, our studies reveal the molecular mechanism by which cannabinoids inhibit tumor growth. We found that aberrant methylation of CB1 represents a clear mechanism for loss of expression in CRC. Using multiple approaches, we provide in vivo evidence demonstrating that endocannabinoid signaling via CB1 plays a key role in regulating intestinal tumor growth. Importantly, we elucidated the signaling pathway that mediates the pro-apoptotic effects of CB1. Moreover, our results may provide a rationale for the development of CB1 agonists that do not cross the blood-brain barrier for cancer prevention or treatment in combination with a demethylating agent."
"Cannabinoids and cancer: pros and cons of an antitumour strategy." 2009 Jan 29 - British Journal of Pharmacology. By Maurizio Bifulco1, Chiara Laezza, Simona Pisanti, and Patrizia Gazzerro. OnlineLibrary.Wiley.com.
"Even if the use of cannabinoids in clinical practice needs further preclinical research, in order to confirme safety, efficacy, doses and administration protocols, the cannabinoids could provide unquestionable advantages compared to current antitumoural therapies: (1) cannabinoids selectively affect tumour cells more than their nontransformed counterparts that might even be protected from cell death; (2) systematically administered selective inhibitors of endocannabinoid degradation would be effective only in those tissues where endocannabinoid levels are pathologically altered, without any significant psychotropic or immunosuppressive activity; (3) selective CB1 agonists unable to cross the blood–brain barrier would be deprived of the immunosuppressive and psychotropic effects of cannabinoids and therefore could be efficaciously used as antineoplastic drugs in a large number of tumours, with the exception of glioma; (4) cannabinoids could represent an efficacious therapy in COX-2-expressing tumours that have become resistant to induction of apoptosis: acting as COX-2-substrates with no effect on the protective properties of COX-2-derived products, they could offer some advantage with respect to the NSAID in order to enhance the sensibility to conventional anticancer therapies."
"Cannabidiol inhibits cancer cell invasion via upregulation of tissue inhibitor of matrix metalloproteinases-1." 2009 Nov - Journal of Biochemical Pharmacology. By Robert Ramer, Jutta Merkord, Helga Rohde, and Burkhard Hinz. ScienceDirect.com.
"Altogether, these findings provide a novel mechanism underlying the anti-invasive action of cannabidiol and imply its use as a therapeutic option for the treatment of highly invasive cancers."
"Cannabidiol inhibits human glioma cell migration through a cannabinoid receptor-independent mechanism." 2009 Jan 29 - British Journal of Pharmacology. By Angelo Vaccani, Paola Massi, Arianna Colombo1, Tiziana Rubino1, and Daniela Parolaro1. OnlineLibrary.Wiley.com.
"In conclusion, the present study demonstrates, for the first time, that CBD can inhibit the migration of tumoral cells. Although the mechanism of this action is not clear at the moment, we can exclude any engagement of classical cannabinoid receptors and/or Gi/o-coupled receptors. Our data further support the use of cannabinoids as antimetastatic drugs as previously demonstrated for met-fluoro-anandamide on rat thyroid cancer cell (Portella et al., 2003). This antimigratory property, together with the known antiproliferative and apoptotic features of CBD (Massi et al., 2004), strengthen the evidence for its use as a potential antitumoral agent."
"Use of cannabinoid receptor agonists in cancer therapy as palliative and curative agents." 2009 Mar 11 - Best Practice & Research Clinical Endocrinology & Metabolism. By Simona Pisanti, Anna Maria Malfitano, Claudia Grimaldi, Antonietta Santoro, Patrizia Gazzerro, Chiara Laezza, and Maurizio Bifulco. ScienceDirect.com.
"Cannabinoids (the active components of Cannabis sativa) and their derivatives have received renewed interest in recent years due to their diverse pharmacological activities. In particular, cannabinoids offer potential applications as anti-tumour drugs, based on the ability of some members of this class of compounds to limit cell proliferation and to induce tumour-selective cell death. Although synthetic cannabinoids may have pro-tumour effects in vivo due to their immunosuppressive properties, predominantly inhibitory effects on tumour growth and migration, angiogenesis, metastasis, and also inflammation have been described. Emerging evidence suggests that agonists of cannabinoid receptors expressed by tumour cells may offer a novel strategy to treat cancer."
"Cannabidiol Enhances the Inhibitory Effects of Tetra9-Tetrahydrocannabinol on Human Glioblastoma Cell Proliferation and Survival." 2010 Jan 12 - Journal of Molecular Cancer Therapeutics. By Jahan P. Marcu1, Rigel T. Christian, Darryl Lau, Anne J. Zielinski, Maxx P. Horowitz, Jasmine Lee1, Arash Pakdel, Juanita Allison1, Chandani Limbad, Dan H. Moore, Garret L. Yount, Pierre-Yves Desprez and Sean D. McAllister. MCT.ACCRJournals.org.
"The treatment of glioblastoma [brain tumor] cells with both [Cannabis] compounds led to significant modulations of the cell cycle and induction of reactive oxygen species and apoptosis as well as specific modulations of extracellular signal-regulated kinase and caspase activities. These specific changes were not observed with either compound individually, indicating that the signal transduction pathways affected by the combination treatment were unique. Our results suggest that the addition of cannabidiol to delta-9-THC may improve the overall effectiveness of delta-9-THC in the treatment of glioblastoma in cancer patients."
"Cannabidiol Induces Programmed Cell Death in Breast Cancer Cells by Coordinating the Cross-talk between Apoptosis and Autophagy." 2011 Jul - Journal of Molecular Cancer Therapeutics. By Ashutosh Shrivastava, Paula M. Kuzontkoski, Jerome E. Groopman, and Anil Prasad. MCT.AACRJournals.org.
"Cannabidiol (CBD), a major nonpsychoactive constituent of cannabis, is considered an antineoplastic agent on the basis of its in vitro and in vivo activity against tumor cells. However, the exact molecular mechanism through which CBD mediates this activity is yet to be elucidated. Here, we have shown CBD-induced cell death of breast cancer cells, independent of cannabinoid and vallinoid receptor activation."
Image: Photograph by louisa_catlover, CC BY-SA 2.0 License