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Thanks gdpawel for your post. It reinforces my long held doubts that the genetic approach is the best in cancer treatment research. On the one hand trying to tackle all oncogenes at the same time is looking as an impossible task (since a master "switch" has yet to be found) which also implies a high probability of adversely affecting the life sustaining processes of normal cells. On the other hand targetting a few genes may lead to a treatment only effective until cancer cells use the neglected genes to grow again. In addition treatments based on a handfull of genes means targetted treatments which also means a lot of research to find the many specialized drugs.
This is why I tended to place more confidence in research of treatments which rely on processes less subject to multiple mutations such as virus based or the control of angiogenesis. Even this latter approach involves the possibility of affecting normal functions as wound healing & pregnancy. The extraordinary results obtained in 1998 on mice treated with the antiangiogenesis combo of Angiostatin+Endostatin have not been tried in humans & may never translate. But even if antiangiogenesis does not provide, in the end, a cure it has a better than average chance to eventually stabilize cancer at a low level devoid of symptoms akin to properly treated type 2 diabetes.
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