{"id":968,"date":"2020-04-09T14:32:09","date_gmt":"2020-04-09T18:32:09","guid":{"rendered":"http:\/\/haidut.me\/?p=968"},"modified":"2020-04-10T11:40:55","modified_gmt":"2020-04-10T15:40:55","slug":"blocking-pufa-supply-halts-brain-cancer-glioblastoma","status":"publish","type":"post","link":"https:\/\/haidut.me\/?p=968","title":{"rendered":"Blocking PUFA supply halts brain cancer (glioblastoma)"},"content":{"rendered":"

Just a few days ago I posted about the strikingly therapeutic effects of vitamin B3 in brain cancer (glioblastoma)<\/a>. The mechanism of action of niacin in that study was deemed to be boosting of the immune system’s ability to recognize the tumor and destroy it. In that post I opined that I suspect niacin’s inhibition of fatty acid oxidation (FAO) to probably be a more reasonable explanation. A day after I made that post I stumbled upon the study below, which corroborates my statement from the niacin post. The study below demonstrates once again the crucial role of PUFA in cancer growth and also provides further evidence that inhibiting either the supply of PUFA to or its oxidation by the tumor<\/a>, can completely halt the growth of various cancer types. In other words, despite oncology’s insistence to the contrary, the evidence accumulated so far strongly suggests that tumors of various organs are essentially the same disease of metabolic origin and as such can be reliably treated through metabolic interventions. More specifically, the study below found that glioblastoma (and likely all other types of cancer) depends on PUFA not only for fuel but also for the stability of lysosomes membranes inside its cells. PUFA is transported inside cells by a so-called fatty-acid binding protein (FABP) 3, also known as mammary-derived growth inhibitor (MDGI). The study demonstrated that MDGI is induced by hypoxia and its expression is much higher in glioblastoma cells compared to normal cells, and that higher expression reliably predicts mortality. Inhibition of that protein leads to PUFA deficiency inside cancer cells and thus to degradation of the lysosomes’ membranes – an effect known clinically as lysosomal membrane permeabilization (LMP). Increasing LMP by MGDI blockade or by administering drugs known to have an LMP effect through another mechanism blocked tumor growth. The LMP inhibitor used by the study was clemastine <\/a>– an old antihistamine with a high-rate of side effects, which may limit its applicability as cancer treatment. However, the study also mentions a number of other drugs with similar therapeutic effects<\/a> and those drugs include the well-known tricyclics such as nortryptiline, amitryptiline and, of course, cyproheptadine<\/strong>.<\/p>\n

Brain Cancer Halted in Mice Using Antihistamine Drug<\/a><\/p><\/blockquote>\n