There exists abundant evidence thatmutations that change the function orexpression of growth-regulatory genescan lead to progression to a cancerousphenotype, and the progressiveaccumulation of such changes as theunderpinning of tumorigenesis formsthe basis for the somatic mutationtheory (SMT) of cancer [1]. At a molecular level, that model of tumorigenesissuggests that progression to a cancerousphenotype can be driven by gain-offunction in growth-promoting oncogenes and/or loss-of-function in growthinhibitory tumor suppressor geneswithin somatic cells (a third class of‘‘stability’’ genes are also a contributorto tumorigenesis [2] but are not considered in this paper). A frequently usedanalogy for that model compares theseclasses of genes to the gas pedal andbrakes of an automobile [2]. However,there is evidence that this model maynot be suf?cient in itself to explain thedevelopment of cancer [3].
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