Abstract
One of the major problems faced by multicellular organisms is the continuous suppression of outgrowth of somatic cells that acquire a growth advantage through mutation. In principle, any somatic cell that acquires a growth advantage should spontaneously outgrow its siblings, spread, invade and so form a tumour. Moreover, clonal expansion of the mutant cell necessarily increases number of targets for additional carcinogenic mutations that would foster tumour progression. Thus, cancer appears to be an inevitable consequence of natural selection within the soma—given enough mutations. In man, this “neoplasia problem” is further exacerbated by three factors: our substantial physical size, our longevity, and the self-renewing (i.e. proliferating) nature of many of our tissues. The larger an organism is, the greater the number of potential cellular targets for neoplastic mutations. Likewise, the longer an organism lives, the greater the chances of neoplasia occurring at some point in its life. Finally, many of our tissues (notably epithelial and haematopoietic) exhibit substantial proliferation throughout our lives so cells within them sustain a risk of de novo mutation throughout life.
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Evan, G.I., Harrington, E.H., McCarthy, N.J., Littlewood, T.D., Hancock, D.C. (1996). The Integrated Control of Cell Proliferation and Cell Viability. In: Mihich, E., Housman, D. (eds) Cancer Genes. Pezcoller Foundation Symposia, vol 7. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-5895-8_1
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