Medical Cannabis and Cancer

Medical cannabis (medical marijuana) has long had a place in treating the symptoms of cancer and the side effects of cancer therapies (e.g., chemotherapy, radiation therapy, cancer surgery).  Examples of common cancer-related symptoms include pain, nausea, vomiting, fatigue, lack of appetite, and weight loss.

Two cannabinoids (dronabinol and nabilone) are FDA approved for the prevention or treatment of chemotherapy-related nausea and vomiting.  A natural sublingual cannabinoid extract (Sativex; equal parts tetrahydrocannabinol and cannabidiol) has clinic trials pending in the U.S. for approval in the treatment of pain associated with cancer.

Cannabis has also been shown to have a direct anti-cancer effect and has been shown to kill cancer cells in the laboratory.

The U.S. government (National Institute on Drug Abuse, NIDA) funded the first study that documented the anti-tumor effects of cannabis.  Results were published in the September, 1975 edition of the Journal of the National Cancer Institute.  The study found that THC slowed the growth of lung cancer and a virus-induced leukemia in laboratory mice, and prolonged their mean survival time by as much as 36 percent.

The U.S. government learned more about marijuana’s anti-cancer effects in a 1997 study by the U.S. National Toxicology Program which concluded that rats and mice treated with THC over long periods of time had greater protection against malignant tumors than those left untreated.

The possible anti-tumor activity of THC in human beings was first shown in a small 2006 pilot study conducted in Spain where THC was administered directly into aggressive glioblastoma multiforme brain tumors.

Research has continued to show favorable outcomes in studies examining the effects of cannabinoid molecules such as THC and CBD on cancer, including brain cancer, thyroid cancer, lymphoma, skin cancer, pancreatic cancer, uterine cancer, breast cancer, and prostate cancer.

Scientifically, there is basis for the use of cannabis in the treatment of cancer.  Two of cannabis’ key medicinal ingredients, tetrahydrocannabinol (THC) and cannabidiol (CBD), haves been documented to have a number of effects on cancer cells in petri dish (in vitro) and animal (in vivo) studies:

  • Anti-proliferative – inhibits cancer cell growth
  • Anti-metastatic – inhibits cancer cells from spreading
  • Anti-angiogenic – inhibits formation of blood vessels that supply tumors
  • Pro-apoptotic – promotes naturally programmed cell death which decreases the likelihood of genetic mutations that can lead to cancer

Cannabinoid molecules exert their actions by binding to cannabinoid receptors (e.g., CB1 and CB2).  These cell membrane receptors are coupled to intracellular pathways that regulate cell growth and survival.

Highlights of Cannabinoid Research from the Scientific Literature

Review Article

Alexander A, et al. (2009) Cannabinoids in the treatment of cancer.

Results:  A mini-review of 51 published scientific concluded that cannabinoids could be useful in the treatment of cancer due to their ability to regulate cellular signaling pathways critical for cell growth and survival.


Brain Cancer

Marcu JP, et al. (2010) Cannabidiol Enhances the Inhibitory Effects of Δ9-THC on Human Glioblastoma Cell Proliferation and Survival.

Results:  The addition of CBD to THC (already shown to be a broad-range cancer inhibitor in cell cultures and in animal studies) may improve the overall effectiveness of THC in the treatment of glioblastoma (brain cancer) patients.

Breast Cancer

McAllister SD, et al. (2010, California Pacific Medical Center Research Institute, San Francisco). Pathways mediating the effects of cannabidiol on the reduction of breast cancer cell proliferation, invasion, and metastasis.  

Results:  Treatment of mice with breast cancer and lung metastases with CBD had significant reduction in the primary tumor mass as well as the size and number of lung metastases. Additionally, CBD down-regulates a gene that regulates the metastatic potential of breast cancer cells.


Colon Cancer

Cianchi F, et al. (2008) Cannabinoid receptor activation induces apoptosis through tumor necrosis factor alpha-mediated ceramide de novo synthesis in colon cancer cells.

Results:  Activation of CB1 and, more efficiently CB2, receptors induced apoptosis (cell death) in colon cancer cell lines.  A CB2 agonist (stimulator) also reduced growth of colon cancer cells in a mouse model of cancer.

Liver Cancer

Xu X, et al. (2006) Overexpression of cannabinoid receptors CB1 and CB2 correlates with improved prognosis of patients with hepatocellular carcinoma.

Results:  Higher numbers of CB1 and CB2 receptors correlates with improved prognosis in patients with hepatocellular carcinoma (liver cancer). Investigators also noted that liver cirrhosis patients who had higher numbers of these receptors also showed an improved prognosis.

Lung Cancer

Preet A, 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.

Results:  Tumor samples from THC-treated animals revealed antiproliferative and antiangiogenic effects of THC.

Conclusion:  “Our study suggests that cannabinoids like THC should be explored as novel therapeutic molecules in controlling the growth and metastasis of certain lung cancers.”

Prostate Cancer

Marcu JP, et al. (2009) Inhibition of human tumor prostate PC-3 cell growth by cannabinoids R(+)-Methandamide (MET) and JWH-015: Involvement of CB2.

Results:  The study of human prostate cancer cells in Petri dishes and in mice with the disease found that the cannabinoid receptor CB2 was involved in the inhibition of prostate cancer cell growth in both of these experimental models.

Although there is currently no evidence that cannabis’ effects on the immune system help the body to fight cancer, CB1 and CB2 will clearly play a role in the future of cancer treatment.  THC and CBD, two of the 100+ cannabinoid molecules found in the marijuana plant, may have specific therapeutic applications. There is also evidence that THC and CBD may together inhibit cancer cell proliferation better than they do individually.


Medical Marijuana Patient Information

Besides smoking, delivery methods for the use of medical cannabis include vaporization, tinctures, teas, and edible products.  Most commonly reported side effects from the use of medical cannabis include dry mouth, red eyes, increased appetite, and tiredness.   There has never been a death attributable to a medical cannabis overdose.  Medical marijuana should be used in consultation with a physician who specializes in cannabinoid medicine.

Other Complementary and Alternative Approaches to Cancer Care

  • Acupuncture
  • Traditional Chinese medicine
  • Mind-body methods
  • Nutritional methods (e.g., conenzyme Q10, antioxidants)
  • Herbal extracts and botanicals

Resources

Medical Literature (US National Library of Medicine/National Institutes of Health)

www.PubMed.gov

Human Clinical Trials (a service of the National Institutes of Health)

www.ClinicalTrials.gov

National Cancer Institute (at the National Institutes of Health), “Cannabis and Cannabinoids (PDQ® )”

www.cancer.gov/cancertopics/pdq/cam/cannabis/patient

Information on CBD (cannabidiol)

www.ProjectCBD.org

References

Alexander A, et al. Cannabinoids in the treatment of cancer. Cancer Letters. 2009;285(1):6-12. http://www.ncbi.nlm.nih.gov/pubmed/19442435

Cianchi F, et al. Cannabinoid receptor activation induces apoptosis through tumor necrosis factor alpha-mediated ceramide de novo synthesis in colon cancer cells. Clinical Cancer Research. 2008; 14(23):7691-7700. http://www.ncbi.nlm.nih.gov/pubmed/19047095

Guzman M, et al. A pilot clinical study of Delta9-tetrahydrocannabinol in patients with recurrent glioblastoma multiforme. British Journal of Cancer. 2006; 95(2):197-203. http://www.ncbi.nlm.nih.gov/pubmed/16804518

Marcu JP, et al. Cannabidiol Enhances the Inhibitory Effects of Delta 9-Tetrahydrocannabinol on Human Glioblastoma Cell Proliferation and Survival. Molecular Cancer Therapeutics. 2010;9(1):180-189. http://www.ncbi.nlm.nih.gov/pubmed/20053780

Olea-Herrero N, et al. Inhibition of human tumor prostate PC-3 cell growth by cannabinoids R(+)-Methandamide (MET) and JWH-015: Involvement of CB2. British Journal of Cancer. 2009;101:940-950. http://www.ncbi.nlm.nih.gov/pubmed/19690545

Preet A, 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. 2008; 27(3):339-346. http://www.ncbi.nlm.nih.gov/pubmed/17621270

McAllister SD, et al. [California Pacific Medical Center Research Institute, San Francisco, CA ] Pathways mediating the effects of cannabidiol on the reduction of breast cancer cell proliferation, invasion, and metastasis. Breast Cancer Research and Treatment. 2011; 129(1):37-47. http://www.ncbi.nlm.nih.gov/pubmed/20859676

Munson AE, et al. [Medical College of Virginia, Richmond, VA] Antineoplastic activity of cannabinoids. Journal of the National Cancer Institute. 1975; 55(3):597-602. http://www.ncbi.nlm.nih.gov/pubmed/1159836

Xu X, et al. Overexpression of cannabinoid receptors CB1 and CB2 correlates with improved prognosis of patients with hepatocellular carcinoma.  Cancer Genetics and Cytogenetics. 2006;171(1):31-38. http://www.ncbi.nlm.nih.gov/pubmed/17074588

About markrabe

Mark L. Rabe, MD, ABIHM Integrative Holistic Medicine Centric Wellness 2308 6th Avenue San Diego, CA 92101 Telephone: (619) 546-0420 Fax: (619) 615-2346 E-Mail: info@CentricWellness.com

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