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Herein, we review the 100 year story of SMT and aspects that show why genes are not just blueprints, how radiation and mutation are associated in a more nuanced view, the proposed risk of cancer and bad luck, and the in vitro and in vivo evidence for a new cancer paradigm.
The somatic mutation theory has been the prevailing paradigm in cancer research for the last 50 years. Its premises are: (1) cancer is derived from a single somatic cell that has accumulated multiple DNA mutations, (2) the default state of cell proliferation in metazoa is quiescence, and (3) cancer …
For a century now, this concept has been kept at the center of the somatic mutation theory (SMT). Boveri’s original SMT was subject to modifications during its centennial course. The current SMT retains the premise that cancer is a cell-based disease in which DNA mutations affect the control of cell proliferation.
Recent reviews 63, 65, 80 have agreed that somatic mutation is likely to be the leading cause of initiation of the carcinogenic process. Berenblum and Shubik 23 provided early evidence of a mutational mechanism in the initiation of cancer.
The somatic mutation theory of carcinogenesis has been the dominant force driving cancer research during the 20th century. In brief, it proposes that successive DNA mutations in a single cell cause cancer (monoclonality).
The transformation of a normal cell into a cancer cell takes place through a sequence of a small number of discrete genetic events, somatic mutations: thus, cancer can be regarded properly as a genetic disease of somatic cells.
The somatic mutation theory (Theory 1) proposes that accumulating mutations in oncogenes and tumour suppressor genes transform cells, leading to unbridled proliferation and cancer.