The quote below, from a news release, is a political statement that is based on incomplete and biased science. Remember, once science is politicized, it is no longer science.
Not true! An overwhelming number of studies exist to firmly support cannabis as all-purpose medicine and very possibly a strong candidate as a cure for cancer, as was originally reported by the National Cancer Institute.
There has never been a single documented primary human fatality from overdosing on cannabis in its natural form in any amount. How’s that for safety!
In addition, cannabis can be vaporized or eaten in sweets, which takes the smoking issue off the table! And as counter-intuitive as its sounds, evidence exists that cannabis offers a mild protective effect against cancer.
In 2001, the Food and Drug Administration (FDA) and the Drug Enforcement Administration thoroughly analyzed the relevant medical, scientific, and abuse data and concluded that marijuana continues to meet the criteria for placement in schedule I of the Controlled Substances Act. The Food and Drug Administration reiterated this determination in April 2006, stating in a news release:
“Marijuana is listed in Schedule I of the Controlled Substances Act (CSA), the most restrictive schedule. The Drug Enforcement Administration (DEA), which administers the CSA, continues to support that placement and FDA concurred because marijuana met the three criteria for placement in Schedule I under 21 U.S.C. 812(b)(1) (e.g., marijuana has a high potential for abuse, has no currently accepted medical use in treatment in the United States, and has a lack of accepted safety for use under medical supervision).
Empirically Based Evidence Supporting Medical Cannabis
by Paul Armentano
NORML Foundation/Senior Policy Analyst
“Cannabinoids possess … anticancer activity [and may] possibly represent a new class of anti-cancer drugs that retard cancer growth, inhibit angiogenesis (the formation of new blood vessels) and the metastatic spreading of cancer cells.” So concludes a comprehensive review published in the October 2005 issue of the scientific journal Mini-Reviews in Medicinal Chemistry.
Not familiar with the emerging body of research touting cannabis’ ability to stave the spread of certain types of cancers? You’re not alone.For over 30 years, US politicians and bureaucrats have systematically turned a blind eye to scientific research indicating that marijuana may play a role in cancer prevention — a finding that was first documented in 1974. That year, a research team at the Medical College of Virginia (acting at the behest of the federal government) discovered that cannabis inhibited malignant tumor cell growth in culture and in mice.
According to the study’s results, reported nationally in an Aug. 18, 1974, Washington Post newspaper feature, administration of marijuana’s primary cannabinoid THC, “slowed the growth of lung cancers, breast cancers and a virus-induced leukemia in laboratory mice, and prolonged their lives by as much as 36 percent.”
Despite these favorable preclinical findings, US government officials dismissed the study (which was eventually published in the Journal of the National Cancer Institute in 1975), and refused to fund any follow-up research until conducting a similar — though secret — clinical trial in the mid-1990s. That study, conducted by the US National Toxicology Program to the tune of $2 million concluded that mice and rats administered high doses of THC over long periods experienced greater protection against malignant tumors than untreated controls.Rather than publicize their findings, government researchers once again shelved the results, which only came to light after a draft copy of its findings were leaked in 1997 to a medical journal, which in turn forwarded the story to the national media.Nevertheless, in the decade since the completion of the National Toxicology trial, the U.S. government has yet to encourage or fund additional, follow up studies examining the cannabinoids’ potential to protect against the spread cancerous tumors.Fortunately, scientists overseas have generously picked up where US researchers so abruptly left off. In 1998, a research team at Madrid’s Complutense University discovered that THC can selectively induce apoptosis (program cell death) in brain tumor cells without negatively impacting the surrounding healthy cells. Then in 2000, they reported in the journal Nature Medicine that injections of synthetic THC eradicated malignant gliomas (brain tumors) in one-third of treated rats, and prolonged life in another third by six weeks. In 2003, researchers at the University of Milan in Naples, Italy, reported that non-psychoactive compounds in marijuana inhibited the growth of glioma cells in a dose dependent manner and selectively targeted and killed malignant cancer cells.
The following year, researchers reported in the journal of the American Association for Cancer Research that marijuana’s constituents inhibited the spread of brain cancer in human tumor biopsies. In a related development, a research team from the University of South Florida further noted that THC can also selectively inhibit the activation and replication of gamma herpes viruses. The viruses, which can lie dormant for years within white blood cells before becoming active and spreading to other cells, are thought to increase one’s chances of developing cancers such as Karposi’s Sarcoma, Burkitts lymphoma, and Hodgkins disease.
More recently, investigators published pre-clinical findings demonstrating that cannabinoids may play a role in inhibiting cell growth of colectoral cancer, skin carcinoma, breast cancer, and prostate cancer, among other conditions. When investigators compared the efficacy of natural cannabinoids to that of a synthetic agonist, THC proved far more beneficial – selectively decreasing the proliferation of malignant cells and inducing apoptosis more rapidly than its synthetic alternative while simultaneously leaving healthy cells unscathed.Nevertheless, US politicians have been little swayed by these results, and remain steadfastly opposed to the notion of sponsoring – or even acknowledging – this growing body clinical research, preferring instead to promote the unfounded notion that cannabis use causes cancer. Until this bias changes, expect the bulk of research investigating the use of cannabinoids as anticancer agents to remain overseas and, regrettably, overlooked in the public discourse.”
The following current research studies all provide overwhelming evidence that THC holds the promise of being a non-toxic multipurpose chemotherapy agent that may have anti-tumor action on many different types of cancer.THC and synthetic cannabinoids both have similar action on CB1/2 receptors, and seem to work best in combination, just as ingesting cannabis as a whole plant produces its wide spectrum healing effects, such as relieving vomiting, being able to eat, having no physical pain and being able to sleep. This is how the body heals itself.
These four medically proven cancer treatment effects of cannabis on their own totally disprove the FDA statement, but with an anti-tumor effect added, as also reported by NCI, this plant becomes a “Swiss survival knife”of medicines. Imagine that — one drug that treats five different medical conditions at once!A quick search of Wikipedia yields the following five studies:”Investigators at Madrid’s Complutense University, School of Biology, first reported that THC induced apoptosis (programmed cell death) in glioma cells in culture”[1a]
“Investigators followed up their initial findings, reporting that the administration of both THC and the synthetic cannabinoid agonist WIN55-212-2 induced a considerable regression of malignant gliomas in animals” [2b]
“Researchers again confirmed cannabinoids’ ability to inhibit tumor growth in animals in 2003″[3c]
“Most Recently investigators at the University of California, Pacific Medical Center reported that cannabinoids possess synergistic anti-cancer properties — finding that the administration of a combination of the plant’s constituents is superior to the administration of isolated compounds alone”[4d]
“Consequently, many experts now believe that cannabinoids may represent a new class of anticancer drugs that retard cancer growth, inhibit angiogenesis and the metastic spreading of cancer cells [5e] and have recommended that at least one cannabinoid, cannabidiol, now be utilized in cancer therapy.”
by Paul Armentano
NORML Foundation/Senior Policy Analyst
Gliomas (tumors in the brain) are especially aggressive malignant forms of cancer, often resulting in the death of affected patients within one to two years following diagnosis. There is no cure for gliomas and most available treatments provide only minor symptomatic relief.
A review of the modern scientific literature reveals numerous preclinical studies and one pilot clinical study demonstrating cannabinoids’ ability to act as anti-neoplastic agents, particularly on glioma cell lines.
Writing in the September 1998 issue of the journal FEBS Letters, investigators at Madrid’s Complutense University, School of Biology, first reported that delta-9-THC induced apoptosis (programmed cell death) in glioma cells in culture. Investigators followed up their initial findings in 2000, reporting that the administration of both THC and the synthetic cannabinoid agonist WIN 55,212-2 “induced a considerable regression of malignant gliomas” in animals. Researchers again confirmed cannabinoids’ ability to inhibit tumor growth in animals in 2003.That same year, Italian investigators at the University of Milan, Department of Pharmacology, Chemotherapy and Toxicology, reported that the non-psychoactive cannabinoid, cannabidiol (CBD), inhibited the growth of various human glioma cell lines in vivo and in vitro in a dose dependent manner.
Writing in the November 2003 issue of the Journal of Pharmacology and Experimental Therapeutics Fast Forward, researchers concluded, “Non-psychoactive CBD … produce[s] a significant anti-tumor activity both in vitro and in vivo, thus suggesting a possible application of CBD as an anti neoplastic agent.”In 2004, Guzman and colleagues reported that cannabinoids inhibited glioma tumor growth in animals and in human glioblastoma multiforme (GBM) tumor samples by altering blood vessel morphology (e.g., VEGF pathways). Writing in the August 2004 issue of Cancer Research, investigators concluded, “The present laboratory and clinical findings provide a novel pharmacological target for cannabinoid-based therapies.”
Five Other Studies Found on pub.Med. Relating to Gliomas
J Clin Invest. 2009 May;119(5):1359-72 Department of Biochemistry and Molecular Biology, Complutense University, Madrid, Spain.
Autophagy can promote cell survival or cell death, but the molecular basis underlying its dual role in cancer remains obscure. Here we demonstrate that delta(9)-tetrahydrocannabinol (THC), the main active component of marijuana, induces human glioma cell death through stimulation of autophagy.
The finding of this study describe a mechanism by which THC can promote the autophagic death of human and mouse cancer cells and provide evidence that cannabinoid administration may be an effective therapeutic strategy for targeting human cancers.
From this study:2. Inhibition of glioma growth in vivo by selective activation of the CB(2) cannabinoid receptor
Neuropharmacology, 2004 Sept., Department of Biochemistry and Molecular Biology I, School of Biology, Complutense University, Avenida Complutense, Madrid, Spain.
Abstract: Gliomas, in particular glioblastoma multiforme or grade IV astrocytoma, are the most frequent class of malignant primary brain tumours and one of the most aggressive forms of cancer. Current therapeutic strategies for the treatment of glioblastoma multiforme are usually ineffective or just palliative. During the last few years, several studies have shown that cannabinoids — the active components of the plant Cannabis sativa and their derivatives –slow the growth of different types of tumours, including gliomas, in laboratory animals.
Remarkably, cannabinoids kill glioma cells selectively and can protect non-transformed glial cells from death. These and other findings reviewed here might set the basis for a potential use of cannabinoids in the management of gliomas.
British Journal of Cancer 2006 Department of Biochemistry and Molecular Biology I, School of Biology, Complutense University, Madrid 28040, Spain
Delta 9-Tetrahydrocannabinol (THC) and other cannabinoids inhibit tumour growth and angiogenesis in animal models, so their potential application as antitumoral drugs has been suggested. However, the antitumoral effect of cannabinoids has never been tested in humans. Here we report the first clinical study aimed at assessing cannabinoid antitumoral action, specifically a pilot phase I trial in which nine patients with recurrent glioblastoma multiforme were administered THC intratumorally.
The patients had previously failed standard therapy (surgery and radiotherapy) and had clear evidence of tumour progression. The primary end point of the study was to determine the safety of intracranial THC administration. We also evaluated THC action on the length of survival and various tumour-cell parameters. A dose escalation regimen for THC administration was assessed. Cannabinoid delivery was safe and could be achieved without overt psychoactive effects. Median survival of the cohort from the beginning of cannabinoid administration was 24 weeks (95% confidence interval: 15-33). 9-Tetrahydrocannabinol inhibited tumour-cell proliferation in vitro and decreased tumour-cell Ki67 immunostaining when administered to two patients. The fair safety profile of THC, together with its possible antiproliferative action on tumour cells reported here and in other studies, may set the basis for future trials aimed at evaluating the potential antitumoral activity of cannabinoids.
Cancer In General
From Paul Armentano at NORML:
In addition to cannabinoids’ ability to moderate glioma cells, separate studies demonstrate that cannabinoids and endocannabinoids can also inhibit the proliferation of other various cancer cell lines, including breast carcinoma,[11-15] prostate carcinoma,[16-18] colorectal carcinoma, gastric adenocarcinoma, skin carcinoma, leukemia cells,[22-23]neuroblastoma, lung carcinoma,[25-26] uterus carcinoma, thyroid epithelioma, pancreatic adenocarcinoma,[29-30], cervical carcinoma, oral cancer, biliary tract cancer (cholangiocarcinoma) and lymphoma.[34-35]
Studies also indicate that the administration of cannabinoids, in conjunction with conventional anti-cancer therapies, can enhance the effectiveness of standard cancer treatments. Most recently, investigators at the University of California, Pacific Medical Center reported that cannabinoids possess synergistic anti-cancer properties — finding that the administration of a combination of the plant’s constituents is superior to the administration of isolated compounds alone.
Consequently, many experts now believe that cannabinoids “may represent a new class of anticancer drugs that retard cancer growth, inhibit angiogenesis and the metastatic spreading of cancer cells.”[38-39]
Studies found on Pub. Med.
1. The stress-regulated protein p8 mediates cannabinoid-induced apoptosis of tumor cells
Cancer Cell. 2006 Apr;9(4):301-12.
Department of Biochemistry and Molecular Biology I, School of Biology, Complutense University, 28040 Madrid, Spain.
One of the most exciting areas of current research in the cannabinoid field is the study of the potential application of these compounds as antitumoral drugs. Here, we describe the signaling pathway that mediates cannabinoid-induced apoptosis of tumor cells. By using a wide array of experimental approaches, we identify the stress-regulated protein p8 as an essential mediator of cannabinoid antitumoral action. Activation of this pathway may constitute a potential therapeutic strategy for inhibiting tumor growth.
2. Cannabis-derived substances in cancer therapy–an emerging anti-inflammatory role for the cannabinoids
Curr Clin Pharmacol. 2010 Nov 1;5(4):281-7.
Division of Cellular and Molecular Medicine (Oncology), St George’s University of London, London, UK. email@example.com
• Cannabinoids, the active components of the cannabis plant, have some clinical merit both as an anti-emetic and appetite stimulant in patients. Recently, interest in developing cannabinoids as therapies has increased following reports that they possess anti-tumour properties.
• Research into cannabinoids as anti-cancer agents is in its infancy, and has mainly focused on the pro-apoptotic effects of this class of agent. Impressive anti-cancer activities have been reported; actions that are mediated in large part by disruptions to ubiquitous signalling pathways such as ERK and PI3-K.
• However, recent developments have highlighted a putative role for cannabinoids as anti-inflammatory agents. Chronic inflammation has been associated with neoplasia for sometime, and as a consequence, reducing inflammation as a way of impacting cancer presents a new role for these compounds. This article reviews the ever-changing relationship between cannabinoids and cancer, and updates our understanding of this class of agent. Furthermore, the relationship between chronic inflammation and cancer, and how cannabinoids can impact this relationship will be described.
3. Cannabinoids for cancer treatment: progress and promise
Neuropharmacology. 2004 Sept
Chemoprevention Program, Paul P. Carbone Comprehensive Cancer Center and Dept of Dermatology, School of Medicine and Public Health, University of Wisconsin, Madison, Wisconsin 53706, USA.
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. Here, we review recent work that raises interest in the development and exploration of potent, nontoxic, and nonhabit forming cannabinoids for cancer therapy.
4. Use of cannabinoid receptor agonists in cancer therapy as palliative and curative agents
Best Pract Res Clin Endocrinol Metab. 2009 Feb.
Department of Pharmaceutical Sciences, University of Salerno, Italy.
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. In this chapter we review the more recent results generating interest in the field of cannabinoids and cancer, and provide novel suggestions for the development, exploration and use of cannabinoid agonists for cancer therapy, not only as palliative but also as curative drugs.
Cannabinoids in the treatment of cancer
Cancer Lett. 2009 Nov 18;285(1):6-12. Epub 2009 May 12.Dept of Pharmacology and Toxicology, University of Otago, Dunedin, New Zealand.
Cannabinoids, the active components of the hemp plant Cannabis sativa, along with their endogenous counterparts and synthetic derivatives, have elicited anti-cancer effects in many different in vitro and in vivo models of cancer. While the various cannabinoids have been examined in a variety of cancer models, recent studies have focused on the role of cannabinoid receptor agonists (both CB(1) and CB(2)) in the treatment of estrogen receptor-negative breast cancer. This review will summarize the anti-cancer properties of the cannabinoids, discuss their potential mechanisms of action, as well as explore controversies surrounding the results.
Inhibition of cancer cell invasion by cannabinoids via increased expression of tissue inhibitor of matrix metalloproteinases-1
J Natl Cancer Inst. 2008 Jan 2;100(1):59-69. Epub 2007 Dec 25.
Institute of Toxicology and Pharmacology, University of Rostock, Schillingallee 70, Rostock D-18057, Germany.
Cannabinoids, in addition to having palliative benefits in cancer therapy, have been associated with anticarcinogenic effects. Although the antiproliferative activities of cannabinoids have been intensively investigated, little is known about their effects on tumor invasion.
We found that increased expression of TIMP-1 mediates an anti-invasive effect of cannabinoids. Cannabinoids may therefore offer a therapeutic option in the treatment of highly invasive cancers.
Cannabinoid receptor as a novel target for the treatment of prostate cancer
Cancer Res. 2005 Mar 1;65(5):1635-41
Department of Dermatology, University of Wisconsin, Madison, Wisconsin 53706, USA.
Cannabinoids, the active components of Cannabis sativa (marijuana) and their derivatives have received renewed interest in recent years due to their diverse pharmacologic activities such as cell growth inhibition, anti-inflammatory effects and tumor regression.
Here we show that expression levels of both cannabinoid receptors, CB1 and CB2, are significantly higher in CA-human papillomavirus-10 (virally transformed cells derived from adenocarcinoma of human prostate tissue), and other human prostate cells LNCaP, DUI45, PC3, and CWR22Rnu1 than in human prostate epithelial and PZ-HPV-7 (virally transformed cells derived from normal human prostate tissue) cells. WIN-55,212-2 (mixed CB1/CB2 agonist) treatment with androgen-responsive LNCaP cells resulted in a dose- (1-10 micromol/L) and time-dependent (24-48 hours) inhibition of cell growth, blocking of CB1 and CB2 receptors by their antagonists SR141716 (CB1) and SR144528 (CB2) significantly prevented this effect. Extending this observation, we found that WIN-55,212-2 treatment with LNCaP resulted in a dose- (1-10 micromol/L) and time-dependent (24-72 hours) induction of apoptosis (a), decrease in protein and mRNA expression of androgen receptor (b), decrease in intracellular protein and mRNA expression of prostate-specific antigen (c), decrease in secreted prostate-specific antigen levels (d), and decrease in protein expression of proliferation cell nuclear antigen and vascular endothelial growth factor (e). Our results suggest that WIN-55,212-2 or other non-habit-forming cannabinoid receptor agonists could be developed as novel therapeutic agents for the treatment of prostate cancer.
The cannabinoid delta(9)-tetrahydrocannabinol inhibits RAS-MAPK and PI3K-AKT survival signalling and induces BAD-mediated apoptosis in colorectal cancer cells
Int J Cancer, 2007 Nov 15;121(10):2172-80.
Department of Cellular and Molecular Medicine, Cancer Research UK, Colorectal Tumour Biology Group, School of Medical Sciences, University of Bristol, University Walk, Bristol, United Kingdom.
Deregulation of cell survival pathways and resistance to apoptosis are widely accepted to be fundamental aspects of tumorigenesis. As in many tumours, the aberrant growth and survival of colorectal tumour cells is dependent upon a small number of highly activated signalling pathways, the inhibition of which elicits potent growth inhibitory or apoptotic responses in tumour cells. Accordingly, there is considerable interest in therapeutics that can modulate survival signalling pathways and target cancer cells for death.
There is emerging evidence that cannabinoids, especially Delta(9)-tetrahydrocannabinol (THC), may represent novel anticancer agents, due to their ability to regulate signalling pathways critical for cell growth and survival. Here, we report that CB1 and CB2 cannabinoid receptors are expressed in human colorectal adenoma and carcinoma cells, and show for the first time that THC induces apoptosis in colorectal cancer cells. These data suggest an important role for CB1 receptors and BAD in the regulation of apoptosis in colorectal cancer cells. The use of THC, or selective targeting of the CB1 receptor, may represent a novel strategy for colorectal cancer therapy.
5d. Natalya, Kogan. “Cannabinoids and cancer”. Mini-Reviews in Medicinal Chemistry 5 (10): 941-952.doi:10.2174/138955705774329555. PMID 16250836
 Guzman et al. 1998. Delta-9-tetrahydrocannabinol induces apoptosis in C6 glioma cells. FEBS Letters 436: 6-10.
 Guzman et al. 2000. Anti-tumoral action of cannabinoids: involvement of sustained ceramide accumulation and extracellular signal-regulated kinase activation. Nature Medicine 6: 313-319.
4] Massi et al. 2004. Antitumor effects of cannabidiol, a non-psychotropic cannabinoid, on human glioma cell lines.Journal of Pharmacology and Experimental Therapeutics Fast Forward 308: 838-845.
5] Guzman et al. 2004. Cannabinoids inhibit the vascular endothelial growth factor pathways in gliomas (PDF). Cancer Research 64: 5617-5623.
 Allister et al. 2005. Cannabinoids selectively inhibit proliferation and induce death of cultured human glioblastoma multiforme cells. Journal of Neurooncology 74: 31-40.
 Guzman et al. 2006. A pilot clinical study of delta-9-tetrahydrocannabinol in patients with recurrent glioblastoma multiforme. British Journal of Cancer (E-pub ahead of print).
8] Parolaro and Massi. 2008. Cannabinoids as a potential new drug therapy for the treatment of gliomas. Expert Reviews of Neurotherapeutics 8: 37-49
 Galanti et al. 2007. Delta9-Tetrahydrocannabinol inhibits cell cycle progression by downregulation of E2F1 in human glioblastoma multiforme cells. Acta Oncologica 12: 1-9.
 Calatozzolo et al. 2007. Expression of cannabinoid receptors and neurotrophins in human gliomas. Neurological Sciences 28: 304-310.
 Cafferal et al. 2006. Delta-9-Tetrahydrocannabinol inhibits cell cycle progression in human breast cancer cells through Cdc2 regulation. Cancer Research 66: 6615-6621.
 Di Marzo et al. 2006. Anti-tumor activity of plant cannabinoids with emphasis on the effect of cannabidiol on human breast carcinoma. Journal of Pharmacology and Experimental Therapeutics Fast Forward 318: 1375-1387.
 De Petrocellis et al. 1998. The endogenous cannabinoid anandamide inhibits human breast cancer cell proliferation. Proceedings of the National Academy of Sciences of the United States of America 95: 8375-8380.
 McAllister et al. 2007. Cannabidiol as a novel inhibitor of Id-1 gene expression in aggressive breast cancer cells.Molecular Cancer Therapeutics 6: 2921-2927.
 Cafferal et al. 2010. Cannabinoids reduce ErbB2-driven breast cancer progression through Akt inhibition.Molecular Cancer 9: 196.
 Sarfaraz et al. 2005. Cannabinoid receptors as a novel target for the treatment of prostate cancer. Cancer Research 65: 1635-1641.
 Mimeault et al. 2003. Anti-proliferative and apoptotic effects of anandamide in human prostatic cancer cell lines.Prostate 56: 1-12.
 Ruiz et al. 1999. Delta-9-tetrahydrocannabinol induces apoptosis in human prostate PC-3 cells via a receptor-independent mechanism. FEBS Letters 458: 400-404.
 Pastos et al. 2005. The endogenous cannabinoid, anandamide, induces cell death in colorectal carcinoma cells: a possible role for cyclooxygenase-2. Gut 54: 1741-1750.
 Di Marzo et al. 2006. op. cit
 Casanova et al. Inhibition of skin tumor growth and angiogenesis in vivo by activation of cannabinoid receptors. 2003. Journal of Clinical Investigation 111: 43-50.
 Powles et al. 2005. Cannabis-induced cytotoxicity in leukemic cell lines. Blood 105: 1214-1221
 Jia et al 2006. Delta-9-tetrahydrocannabinol-induced apoptosis in Jurkat leukemic T cells in regulated by translocation of Bad to mitochondria. Molecular Cancer Research 4: 549-562.
 Preet et al. 2008. Delta9-Tetrahydrocannabinol inhibits epithelial growth factor-induced lung cancer cell migration in vitro as well as its growth and metastasis in vivo. Oncogene 10: 339-346.
 Baek et al. 1998. Antitumor activity of cannabigerol against human oral epitheloid carcinoma cells. Archives of Pharmacal Research: 21: 353-356.
 Carracedo et al. 2006. Cannabinoids induce apoptosis of pancreatic tumor cells via endoplasmic reticulum stress-related genes. Cancer Research 66: 6748-6755.
 Michalski et al. 2008. Cannabinoids in pancreatic cancer: correlation with survival and pain. International Journal of Cancer 122: 742-750.
 Ramer and Hinz. 2008. Inhibition of cancer cell invasion by cannabinoids via increased cell expression of tissue inhibitor of matrix metalloproteinases-1. Journal of the National Cancer Institute 100: 59-69.
 Whyte et al. 2010. Cannabinoids inhibit cellular respiration of human oral cancer cells. Pharmacology 85: 328-335.
 Leelawat et al. 2010. The dual effects of delta(9)-tetrahydrocannabinol on cholangiocarcinoma cells: anti-invasion activity at low concentration and apoptosis induction at high concentration. Cancer Investigation 28: 357-363.
 Gustafsson et al. 2006. Cannabinoid receptor-mediated apoptosis induced by R(+)-methanandamide and Win55,212 is associated with ceramide accumulation and p38 activation in mantle cell lymphoma. Molecular Pharmacology 70: 1612-1620.
 Gustafsson et al. 2008. Expression of cannabinoid receptors type 1 and type 2 in non-Hodgkin lymphoma: Growth inhibition by receptor activation. International Journal of Cancer 123: 1025-1033.
 Liu et al. 2008. Enhancing the in vitro cytotoxic activity of Ä9-tetrahydrocannabinol in leukemic cells through a combinatorial approach. Leukemia and Lymphoma 49: 1800-1809.
 Marcu et al. 2010. Cannabidiol enhances the inhibitory effects of delta9-tetrahydrocannabinol on human glioblastoma cell proliferation and survival. Molecular Cancer Therapeutics 9: 180-189.
 Sarafaraz et al. 2008. Cannabinoids for cancer treatment: progress and promise. Cancer Research 68: 339-342.
Editor’s note: Ron Marczyk is a retired high school health eduation teacher who taught Wellness and Disease Prevention, Drug and Sex Ed, and AIDS education to teens aged 13-17.
He also taught a high school International Baccalaureate psychology course. He taught in a New York City public school as a Drug Prevention Specialist.
He is a Registered Nurse with six years of ER/Critical Care experience in NYC hospitals, earned an M.S. in cardiac rehabilitation and exercise physiology, and worked as a New York City police officer for two years.
Currently he is focused on how evolutionary psychology explains human behavior.