As states pass laws allowing the use of medical and now even recreational use of cannabis, many issues arise. While opponents have always been quick to point out that DUID is a serious concern connected to legalization, studies are finally showing hard numbers related to actual risk factors. Unfortunately, much of what has been ascertained about the effects of marijuana on people is anecdotal, as very little clinical research been approved or run on human subjects—however, relatively recent findings may warrant more clinical research and perhaps phase I trials involving human test subjects, as scientists, and particularly oncologists, search for a cure for cancer.


Cannabinoids Contribute to Apoptosis in Tumors

Medical marijuana has empirically been used to help cancer patients in a palliative manner (i.e. appetite stimulation, and inhibition of nausea and emesis/vomiting), although it has been known for about 40 years now that cannabinoids may actually be able to play a role in destroying tumors instead of just easing pain while other antiproliferative drugs attempt to clear the cancer. A study in the 1970s discovered as much. Research didn’t really pick up again until the 90s, when it was discovered that the reason cannabinoids cause apoptosis (cell-death) had something to do with CB1 and CB2 receptors, and that cannabinoids were effective at destroying many varieties of tumors including lymphomas, lung and skin carcinomas, gliomas, and thyroid epitheliomas, and has even shown very recently to help cure Crohn’s disease. Dr. Raymond DuBois and his team of doctors and scientists can now add colorectal tumors to that list.

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Colorectal Cancers Grow in Absence of CB1 Receptors

By xenotransplanting cancerous human colorectal tumors onto nude mice, DuBois and his team came to find that colorectal cancer is able to grow and flourish when CB1 receptors are turned off in cells. Because endocannabinoid signaling has been shown to prevent inflammation in the colon, which is a risk factor for colorectal cancer, DuBois decided to start his work in that area. What he found was that in about ninety percent of his specimens, the gene that encodes CB1 proteins had been chemically stifled by the attachment of methyl groups. Treating the specimens with a demethylating agent called decitabine helped to restore expression to the CB1 gene.

Introduction of Cannabinoids Reduces number of Polyps

After the decitabine had done its work, DuBois and his group introduced an endocannabinoid agonist to his specimen so that it would bind with the now-free CB1 receptors. The group found that, amazingly, the size and number of polyps in their specimen declined anywhere from 16.7 to 50 percent, with greater reduction in the larger-sized polyps. DuBois and his team also found that in mice with CB1 receptors shut off, or that were bound by a CB1 antagonist (one such antagonist is marketed as “rimonabant” for weight loss), the number of precancerous polyps and large growths increased by 3 to 10 times.

Curbing Survivin Induces Cell Death in Tumors

The team discovered that the reason that cannabinoids and CB1 are able to induce apoptosis in cancerous cells is that CB1 smothers a different protein called survivin. Normal human tissue has extremely miniscule amounts of survivin in it, however, the large majority of human tumors sees survivin greatly overexpressed. By identifying a cell signaling pathway by which functioning CB1 receptors minimizes survivin, the researchers correctly identified a molecular mechanism that had previously been shrouded in mystery.

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Implications for the Future

The conclusion here is that we may be one step closer to a cure for cancer, especially colorectal cancer if the patient were to receive some kind of demethylating treatment to reactive CB1 receptors in the growth, and then a cannabinoid to bind to those receptors and eliminate survivin. Actual clinical research and trials may be awhile away, but another study is showing promise by introducing cannabinoids to combat breast cancer that you can read about here.

Written by:

Andrew Heikkila

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