Abstract

For over a century, the somatic mutation theory of carcinogenesis (SMT) has been adopted by researchers as the theory of record to explain the vast bio-medical implications of the cancer disease. Central to this theory is the notion that mutated alleged cancer genes are responsible for the cancer phenotype(s). Despite generous sustained funding and unwavering research commitments, the presence and the roles of genomic mutations remain undefined and controversial. Our analysis of the merits of causatively linking mutated cancer genes and cancer phenotypes suggests that such mutations are neither necessary nor sufficient.

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