Glioblastoma is a destructive and aggressive form of cancer affecting the brain and spinal cord with a grim prognosis. Even after treatment with radiation and chemotherapy, most patients only live an average of 15 months (abta.org). There is no cure for gliomas (brain tumors) and the current treatment provides only minor relief. With such a bleak outlook, it is imperative that medical researchers identify and create an alternative therapy. While the current legal status in the U.S.makes studies on medical cannabis difficult, for more than two decades now researchers in Spain and the United Kingdom have been dutifully studying the effects of cannabis on brain tumors and their results are nothing short of miraculous. These researchers have shown evidence that medical cannabis, also known as medical marijuana, leads the cancer cells to stop growing and eventually causes cellular apoptosis-or cell death. When working in tandem with chemotherapy medications, medical cannabis enhanced the programmed cell death, also known as autophagy, in brain tumors without damaging the surrounding healthy brain tissue.
Since as early as 1998, a medical research team at the Complutense University of Madrid has been studying the effects of cannabinoids such as Tetrahydrocannabinol (THC) and Cannabidiol (CDB). This team, led by Professors Guillermo Velasco and Manuel Guzman published their 1998 study on the effects of THC and other cannabinoids on glial cells and found that THC, “induced apoptosis in several transformed neural cells but not in primary astrocytes or neurons” (Guzman, et al.) The researchers found again, in 2002, that cannabinoids, “induced a considerable regression of malignant gliomas” (Galve-Roperh, et al), and cemented their research in 2003 with findings that cannabis showed an amazing ability to inhibit glioma tumor growth (Blázquez, et al., 2003).
The following year, medical cannabis researchers discovered that cannabis alters the genetic profile of Vascular Endothelial Growth Factor. Vascular Endothelial Growth Factor, also known as VEGF, is a compound used to help grow new blood vessels. In order for the tumor to increase in size, the cells must create new a new vascular supply for purposes of waste disposal, the exchange of gases, and cellular nutrition. When the researchers introduced cannabinoid medications, the VEGF pathways were altered which led to a reduction of blood supply to the tumor. In other words, by altering the ability of the tumor to access its blood supply, cannabis stops the tumor from growing (Blázquez, et al., 2004).
Another major breakthrough in medical cannabis research occured when it was discovered that cannabinoids lead to cellular death in cancer. In addition to halting the growth of tumors and cutting off access to their blood supply, cannabis leads to the cells self-destructing in a process that scientists refer to as “programmed cell death”. The cells die via apoptosis and autophagy, which are normally occurring processes in non-cancerous cells. Generally, cancer cells do not normally self-destruct under these processes and instead continue to grow in size, leading to disastrous consequences. However, medical cannabis researchers have found that when treated with cannabinoids the cancer cells did, in fact, miraculously begin the process of undergoing autophagy or, in other words, the cells began to digest themselves. In a study published in The Journal of Investigation, Dr. Velasco stated: “We actually discovered a new mechanism by which cannabinoids activate a signalling pathway that involves what we call autophagy, which would be like the self-digestion of the cells. So, actually, when cannabinoids are binding to the cells, they trigger a cell-signalling mechanism” (Salazar, et al.) Amazingly, this cell death only occured in the cancer cells and did not affect any of the surrounding healthy cells which remained unharmed. This same research group also found that in addition to autophagy, there is evidence enough to conclude that medical cannabis also leads to cellular apoptosis, or cell death, in glioma cells (Sánchez, et al.).
Scientific investigators at California Pacific Medical Center Research Institute announced that the application of the cannabinoid THC on glioblastoma cells decreased the rapid reproduction of malignant cancer cells. Additionally, THC led to the induction of cell death more rapidly than when the cells were treated with a synthetic cannabinoid known as WIN 55,212-2 (McAllister, et al.). The researchers also noticed that thewhole-molecule THC was selectively targeting the malignant glioblastoma cells while ignoring the healthy surrounding cells in a more discerning manner than the cells treated with the synthetic cannabinoid. In yet another fascinating clinical discovery published by the American Association for Cancer Research, the scientists reported that THC in combination with the chemotherapy drug temozolomide (TMZ), “enhanced autophagy” (Torres, et al.), or programmed cell death, in malignant brain cells that were otherwise resistant to the conventional anticancer treatments widely available. So medical cannabis, in conjunction with chemotherapy, killed glioblastoma more effectively than chemotherapy alone.
While glioblastoma is a particularly aggressive malignant form of cancer, medical research is showing that it does not need to be a death sentence. Medical cannabis, especially when in the form of whole molecule and organic plant-based medicine, outperformed the synthetic cannabinoid medications and even chemotherapy when attacking cancerous cells. These medical researchers are giving hope to patients everywhere that not only does medical cannabis stop the growth of glioblastoma tumors by limiting their access to blood supplies, but the cannabinoids directly correlate to the cellular death of these cancer cells. When combined with conventional chemotherapy, cannabis increased its efficiency in fighting cancer-even for the most stubborn cells.
Written by: Mara Trivino ©KingHarvest.org
1.”Glioblastoma (GBM).” Glioblastoma (GBM) | American Brain Tumor Association, American Brain Tumor Association, 2014, www.abta.org/brain-tumor-information/types-of-tumors/glioblastoma.html?referrer=https%3A%2F%2Fwww.google.com%3Freferrer.
2. Guzman, Et al. “Δ9-Tetrahydrocannabinol Induces Apoptosis in C6 Glioma Cells.” FEBS Letters, No Longer Published by Elsevier, 20 Oct. 1998, www.sciencedirect.com/science/article/pii/S0014579398010850.
3. Galve-Roperh, Ismael, et al. “Anti-Tumoral Action of Cannabinoids: Involvement of Sustained Ceramide Accumulation and Extracellular Signal-Regulated Kinase Activation.” Nature News, Nature Publishing Group, 1 Mar. 2000, www.nature.com/articles/nm0300_313.
4. Blázquez, C, et al. “Inhibition of Tumor Angiogenesis by Cannabinoids.” FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology., U.S. National Library of Medicine, Mar. 2003, www.ncbi.nlm.nih.gov/pubmed/12514108.
5. Blázquez, Cristina, et al. “Cannabinoids Inhibit the Vascular Endothelial Growth Factor Pathway in Gliomas.” Cancer Research, American Association for Cancer Research, 15 Aug. 2004, cancerres.aacrjournals.org/content/64/16/5617. 6. Salazar, María, et al. “Cannabinoid Action Induces Autophagy-Mediated Cell Death through Stimulation of ER Stress in Human Glioma Cells.” The Journal of Clinical Investigation, American Society for Clinical Investigation, 1 May 2009, www.ncbi.nlm.nih.gov/pmc/articles/PMC2673842/.
7. Sánchez, C, et al. “Delta9-Tetrahydrocannabinol Induces Apoptosis in C6 Glioma Cells.”FEBS Letters., U.S. National Library of Medicine, 25 Sept. 1998, www.ncbi.nlm.nih.gov/pubmed/9771884.
8. McAllister, S D, et al. “Cannabinoids Selectively Inhibit Proliferation and Induce Death of Cultured Human Glioblastoma Multiforme Cells.” Journal of Neuro-Oncology., U.S. National Library of Medicine, Aug. 2005, www.ncbi.nlm.nih.gov/pubmed/16078104?dopt=Abstract.
9. Torres, Sofía, et al. “A Combined Preclinical Therapy of Cannabinoids and Temozolomide against Glioma.” Molecular Cancer Therapeutics, American Association for Cancer Research, 1 Jan. 2011, mct.aacrjournals.org/content/10/1/90.