Abstract
Cancer is a consequence of multi-cellularity and is a striking example of multilevel selection. The theory of cancer initiation and progression has its root deep within the evolutionary and ecological concepts. Cancer develops through somatic evolution, with genetic and epigenetic precariousness, generating fitness variation among the cells in the body. Epidemiological, genetic, and molecular biological research have cumulatively provided us with a brimming source of data that affirms our current understanding of the etiology and molecular pathogenesis of cancer. But this aspect only focuses on immediate mechanisms and does not competently explain the pervasiveness of tumors and cancer in animal species or what seems to be the exceptional vulnerability of Homo sapiens. At a practical level, analyses suggest that, for evolutionary reasons, as a species, we are inherently more likely to develop cancer (than we might like to admit). Though we cannot reverse our genetic legacies and predilection to cancer, emphasizing inherent vulnerability in an ‘evolutionary’ way strongly ratifies our current attempts to combat cancer. In actuality, neoplasms are microcosms of evolution. Within a neoplasm, a mosaic of mutant cells competes for space and resources, evades predation by the immune system, and can even cooperate to disperse and colonize new organs (metastasis). The evolution of neoplastic cells can explain both why we get cancer and why it has been so difficult to find a cure. Although the idea of cancer as an evolutionary problem is not new at least historically little attention has been delivered to applications of evolutionary biological principles in understanding and controlling neoplastic progression. Already, we have reached the high time when this should be changed. Ernst Mayr aptly said that “No biological problem is solved until both the proximate and the evolutionary causation has been elucidated” Keywords: [Cancer, adaptation, evolution].
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