Cannabis -vs- Esophageal Cancer
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2828614/: The role of inflammation in evolution of certain types of cancer has been strongly suggested, linking the inflammatory response to 15–20% of all deaths from cancer worldwide . The hallmarks of cancer-related inflammation include the presence of inflammatory cells in tumor tissue, and the regulation of tumor growth, metastasis and angiogenesis by inflammatory mediators (e.g., chemokines, cytokines and prostaglandins). The connection between inflammation and cancer is now generally accepted and nonsteroidal anti-inflammatory drugs have been shown to reduce varied cancer risk. Use of these drugs reduces colon cancer risk by 40–50% and is indicated to be preventative for lung, esophagus and stomach cancer . Hence, inflammation can be considered as a therapeutic opportunity in certain types of cancer. Recent applications of cannabinoids have been extended as antitumor agents [1,88], which relies on their ability to inhibit tumor angiogenesis  or induce direct apoptosis or cell cycle arrest in neoplastic cells [89–92]. A focus on the antiproliferative effects of these compounds in various tumors, such as breast and prostate cancers, pheochromocytoma and malignant gliomas, has been proposed [1,92–94]. Our laboratory reported that, in vitro, THC and other cannabinoids could induce apoptosis in transformed murine and human T cells , including primary acute lymphoblastic human leukemia cells. Furthermore, the treatment of mice bearing a T-cell leukemia with THC could cure approximately 25% of the mice . We further showed that treatment with THC caused interruption of the MAPK/ERK kinase/ERK signaling module that was required for apoptotic lethality [96,97]. The role of endocannabinoids as potential endogenous tumor growth inhibitors has been suggested in a study where it was observed that levels of both AEA and 2-AG were higher in precancerous polyps than in fully developed carcinomas in the colon . Recent in vivo studies proposed that selective targeting of CB2 receptors resulted in colorectal tumor growth inhibition via apoptosis, which was mediated through the stimulation of ceramide . In a xenograft model of thyroid cancer, substances that blocked endocannabinoid degradation also increased the levels of AEA and 2-AG in the tissue and reduced tumor growth . Various attempts have been made to inactivate cannabinoid-degrading enzymes, thereby increasing the local concentration of endocannabinoids at the tumor cell surface. This leads to anti-tumor effects of CB receptor signaling in various cancer types, such as thyroid, brain and prostate cancer [99–103]. Although the majority of the effects of cannabinoids are CB receptor mediated, AEA has been shown to induce its effects on cancerous cells by interacting with TRPV1 receptor [104,105] or cholesterol-rich lipid rafts . Furthermore, it has been reported that signaling pathways are differentially regulated by cannabinoids in normal cells versus cancer cells. In malignancies, such as thyroid cancer, lymphoma, melanoma, pancreas and breast cancer, the levels of cannabinoid receptors are often higher in the tumor compared with normal cells of the same origin, resulting in increased sensitivity to cannabinoids in the malignancies [89,107–110]. Moreover, many animal studies have reported antiproliferative and pro-apoptotic effects of cannabinoids on tumor cells but not on normal tissue [89,91]. Thus, the role of the cannabinoid system in cancer indicates that this system is involved in regulating many of the functions that are essential in cancer development.
https://www.ncbi.nlm.nih.gov/pubmed/20516734: The primary cannabinoids, Delta(9)-tetrahydrocannabinol (Delta(9)-THC) and Delta(8)-tetrahydrocannabinol (Delta(8)-THC) are known to disturb the mitochondrial function and possess antitumor activities. These observations prompted us to investigate their effects on the mitochondrial O(2) consumption in human oral cancer cells (Tu183). This epithelial cell line overexpresses bcl-2 and is highly resistant to anticancer drugs. These results show the cannabinoids are potent inhibitors of Tu183 cellular respiration and are toxic to this highly malignant tumor.