[Editor’s note: This post is excerpted from this week’s forthcoming NORML weekly media advisory. To have NORML’s news alerts and legislative advisories delivered straight to your in-box, sign up here.]
The administration of non-psychotropic plant cannabinoids, in particular cannabidiol (CBD), inhibit proliferation and selectively trigger cell suicide of prostate carcinoma, according to preclinical data to be published in the British Journal of Pharmacology. (Read the study abstract online here.)
An international team of investigators from Italy and the United Kingdom assessed the anti-cancer properties of various non-psychoactive synthetic and botanical cannabinoids, including CBD, CBG (cannabigerol), CBN (cannabinol) and THCV (tetrahydrocannabivarin), in vivo and in vitro (in culture).
Researchers reported, “The … data presented here allow us to suggest that non-THC cannabinoids, and CBD in particular, retard proliferation and cause apoptosis (programmed cell death) of prostate carcinoma growth via a combination of cannabinoid receptor-independent cellular and molecular mechanisms. … We suggest that non-THC cannabinoids … might provide the basis for the development of novel therapeutic strategies for the treatment of prostate carcinoma.”
Prostate cancer is the second most common cancer in American men. It is the second leading cause of cancer death in American males, trailing only behind lung cancer.
Authors of the study concluded, “[T]he effects reported here, together with previously reported cannabinoid receptor-mediated effects of THC on PCCs (prostate carcinoma cells), might provide momentum to clinical studies on cannabinoids and cannabis extracts as a therapy for human prostate carcinoma, either in addition to currently used treatments, or as stand alones, as suggested also by our present in vivo data.”
A separate study of cannabinoids on prostate cancer published in the present edition of the Indian Journal of Neurology also concluded, “Prostate cancer cells possess increased expression of both cannabinoid 1 and 2 receptors, and stimulation of these results in decrease in cell viability, increased apoptosis, and decreased androgen receptor expression and prostate-specific antigen excretion. … It is our conclusion that it would be of interest to conduct clinical trials involving medicinal cannabis or other cannabinoid agonists, comparing clinical markers such as PSA with controls, especially in men with bone metastatic prostate cancer, whom would not only benefit from the possible anti-androgenic effects of cannabinoids but also from analgesia of bone pain, improving quality of life, while reducing narcotic consumption and preventing opioid dependence.”
Cannabinoids and endocannabinoids have been consistently shown to be potent anti-cancer inhibitors in preclinical models, halting the proliferation of glioma cells, breast carcinoma, lung carcinoma, and lymphoma, among other cancer cell lines. NORML’s literature review of this data appears here.
Full text of the study, “Non-THC cannabinoids counteract prostate carcinoma growth in vitro and in vivo: pro-apoptotic effects and underlying mechanisms,” will appear in the British Journal of Pharmacology.
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