Targeted Gene Therapy to Cure Cancer and Some Alternative Approaches that Also Help Slow Aging

Targeted Gene Therapy To Counter High Levels of VEGF

Targeted Gene Therapy To Counter High Levels of VEGF

This is an extremely complex picture of how gene’s help cancer cells grow.  Faults in two types of genes cause cancer: oncogenes, which drive the growth of cancer cells, and tumor suppressor genes, which prevent cancer from developing. The concept of the targeted gene therapy is to attack the most vulnerable parts of the cancer cells based on the person’s specific genes that are causing the growth of cancer cells and the genes that have been turned off preventing tumor suppression.   The four boxes in red are the chemo drugs my Mom is taking to cause cancer cell suicide based on aging gene dysfunction that enabled this brain tumor to exist in the first place.  At the Burzynski Research Clinic, they made this determination by taking a blood sample looking for specific gene markers that told them which genes were turned on and which were turned off causing the growth of her brain tumor.  The one cell growth factor that I have been studying is the mTOR protein.   Inhibiting mTOR slows aging.   The one drug my Mom is taking to stop mTOR (and stop the cancer cell proliferation) is Afinitor.  Several other substances inhibit mTOR in cell cultures – curcumin, EGCG (in green tea), caffeine, and resvratrol (in red wine and grape juice). (Beevers C, Li F, Liu L, Huang S (2006). “Curcumin inhibits the mammalian target of rapamycin-mediated signaling pathways in cancer cells”. Int J Cancer 119 (4): 757–64.) You have to consume a lot of curcumin to kill the cancer cells – but it is physiological possible according to the research – “Phase I clinical trials have shown that high doses (8 g/day) of curcumin can be delivered to patients, yielding 1.77 ± 1.87 μM average peak serum concentration, with virtually no deleterious side effects.  We observed complete abolition of S6K1 and 4E-BP1 phosphorylation and reduced levels of mTOR phosphorylation/autophosphorylation upon 2 h treatment with 2.5 μM curcumin. Our results suggest that the lowest concentration of curcumin that could possibly affect these critical phosphorylation events is well within the range of physiologically achievable concentrations of the compound in cancer patients.”

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