Cancer cells are preferentially killed by anticancer agents because key signals for growth and cell division are "always on" as opposed to the alternative "on" and "off" signaling of normal cells. Too much of today's anticancer drug discovery effort may go toward reversing genetically promoted "always on" signals. More effective anticancer drug targets may be found through use of RNAi technologies that pinpoint the key gene regulatory and metabolic weakness of the "always on" cancer cells.
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James D. Watson (2011) studied this question.
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