I am evaluating whether I should incorporate THC into my cocktail regimen. I have come across some studies showing that some genes expressed in tumors can either negate the anti-cancer effects of THC or even accelerate the proliferation of the cancer because of the THC. https://www.sciencedirect.com/science/article/pii/S0278584615001190. This article discusses growth factor midkine (MDK), the anaplastic lymphoma receptor tyrosine kinase (ALK), and epidermal growth factor receptor (EGFR).
Does anyone know how conclusive these studies are on which pathways glioblastomas may proliferate because of THC? More specifically, is anyone aware of any updates since this paper or other research that shows different results? I am EGFR amplified and obviously don't want to pour gasoline on the fire.
There are a number of in vitro cell culture studies showing variable effects of cannabinoids, some even showing slightly increased proliferation. Studies of this sort typically use drug concentrations far in excess of what is achievable in the body.
ReplyDeleteThe most compelling support for cannabinoids comes for the clinical trial for recurrent GBM where Sativex (CBD:THC, 1:1) was combined with dose intense temozolomide, which achieved significantly improved survival versus chemo alone, even though this was a small trial.
The majority of GBM tumors have EGFR alterations (mutations, amplification, overexpression). EGFR is one of the most prominently active receptor tyrosine kinases in GBM. If cannabinoids were counterindicated for EGFR-driven tumors, we probably wouldn't have seen such positive results in the clinical trial I just mentioned. Larger studies are hopefully forthcoming.
See this post and recent comments:
http://btcocktails.blogspot.com/2017/07/sativex-thc-cbd-plus-temozolomide-for.html
It would be interesting to combine cannabinoid-based treatment with EGFR inhibitors, especially if brain-penetrant EGFR inhibitors could be developed.