Carcinogenesis: An Alternative Hypothesis Comparing Mutagenic Versus Metabolic Models

Carcinogenesis, while traditionally attributed to the accumulation of driver mutations in genes regulating cell proliferation and apoptosis, may also be explored as a consequence of fundamental metabolic reprogramming, an idea catalyzed by the Warburg effect, where cancer cells exhibit a paradoxical preference for glycolysis over the far more efficient oxidative phosphorylation. This implies that metabolic dysregulation may be a primary instigator of neoplastic transformation. Our hypothesis proposes that the abrupt loss of cellular energy may stimulate an atavistic response, wherein rapid proliferation and migration are triggered to enhance survival in fluctuating environments. These responses lead to pathological angiogenesis and unchecked cell growth, thereby bridging the gap between genetic and metabolic pathways of carcinogenesis.