ABSTRACT

INTRODUCTION e transition from normal tissue to invasive cancer is a multistep process in which increasingly malignant cellular populations emerge over time (1-3), generally coincident with accumulating genomic mutations. is is oen described as “somatic evolution” (4-5) because it appears formally analogous to Darwinian evolution in nature. While this conceptual model is well accepted, the interactions with phenotypic properties and environmental selection forces that determine individual tness remain ill dened. Furthermore, the language of evolution is oen employed in carcinogenesis without full explanation. For example, it is oen stated that, during carcinogenesis, some random mutations “confer a selective growth advantage” resulting in clonal expansion and subsequent tumor growth.