What we know, what we don’t, and why we’re still behind on funding
The field of oncology has made significant advancements over the past few decades. The advent of personalized therapy has made possible the identification of certain genes that either increase the risk of developing certain cancer types or allow for therapeutic targeting. And now, with immunotherapies, researchers can harness the power of the body’s own immune system to tackle cancer cells head on.
Despite these enormous advancements in research, receiving a cancer diagnosis remains daunting because we still have no cure.
Evidence supporting the anti-cancer effects of cannabinoids was first reported in 1975 but that lead went cold following prohibition.  In fact, while the National Institutes of Health provides around $6-7 billion in funding for cancer research each year, in 2019, only about $200 million was made available to scientists studying cannabinoids. And while the FDA has approved synthetic cannabinoids to alleviate side effects associated with cancer treatments, no compounds have been approved for cancer itself owing to lack of research–the chicken and egg problem continues.
But a greater understanding of the potential therapeutic contribution of cannabinoids to cancer treatment lies within the endocannabinoid system and the role it plays in supporting a healthy immune system.
The cannabinoid 2 (CB2) receptor is most densely expressed on immune cells, and its highest level of expression can be found on B cells, which play an integral role in fighting off foreign invaders.  In addition to supporting a healthy immune system, cannabinoid 1 (CB1) and CB2 receptors may play more direct roles in cancer.
Let’s look at the potential mechanisms through which cannabinoids may exert anti-cancer effects.
Activation of the CB1 receptor can reduce the proliferation (growth) of pancreatic cancer cells. In fact, both human breast and pancreatic cancer cells have higher levels of CB1 receptor expression compared to healthy cells. 
Other studies have indicated that tetrahydrocannabinol can induce apoptosis, or programmed cell death, in glioma and prostate cancer cells, thereby reducing the spread of cancer cells. 
When tumors are growing, they need a steady blood supply to survive. And a few cancer treatments work by starving tumors.
Studies have shown that endocannabinoids can do this too, in glioma, skin, and thyroid carcinoma, by blocking activation of the vascular endothelial growth factor, which promotes the growth of blood vessels.  In addition, they can inhibit proliferation of endothelial cells, breaking the structure and support of newly forming blood cells. 
Treating cancer is incredibly challenging because cancer cells can break off from a solid tumor and migrate to other parts of the body to grow additional tumors, a process known as metastasis.
Cannabidiol (CBD) has increased levels of ceramide, which suppresses tumor growth.  CBD can also reduce tumor cell invasion and metastasis by increasing levels of intercellular adhesion molecule 1, which plays an important role in the immune system. 
It’s important to note that much of this research was conducted in vitro, or in a dish. And it’s been challenging to replicate some results in pre-clinical models. However, there are many clinical trials underway, with some reporting preliminary positive findings. But, until we learn more, be sure to discuss integrating cannabis use into your current treatment plan with your doctor before initiating use.
- Dariš, B, et al., “Cannabinoids in Cancer Treatment: Therapeutic Potential and Legislation.” Bosnian Journal of Basic Medical Sciences,vol.19, no.1, 2019, pg. 14-23.(impact factor: 1.458; cited by: 12)
- Bifulco, M., & Di Marzo, V., “Targeting The Endocannabinoid System In Cancer Therapy: A Call For Further Research.” Nature Medicine, vol.8, no.6, 2002, pg. 547-550. (impact factor: 30.641; cited by: 183)
- Śledziński, P., et al., “The Current State And Future Perspectives Of Cannabinoids In Cancer Biology.” Cancer Medicine,vol.7, no.3, 2018, pg. 765-775. (impact factor: 3.362; cited by: 15)