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Roles of evolution, quantum mechanics and point mutations in origins of cancer.

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The fact point genetic lesions--which provide the species with an ability to respond favorably to changing environmental conditions--are also specifically compatible with "activating" point mutation sensitive, evolutionarily conserved proto-oncogenes and gene p53 implies an additional function for evolutionary processes. In particular, this suggests that evolutionary point lesions may also be designed to remove from the gene pool those genomes which have accumulated advanced levels of evolutionary-induced mutations, thereby protecting the species from the adverse consequences of accumulating mutations beyond an unsafe upper limit. This hypothesis is used to construct a mutation model polynomial for incidence of human cancer as a function of age. The model assumes that point lesion sensitive proto-oncogenes and "p53-type" genes are evolutionarily conserved and must exhibit wild-type genetic information at fertilization for proper growth. Subsequently, evolutionary lesions populate these conserved domains, eventually causing point lesion sensitive genes to yield amino acid substituted proteins capable of participation in transforming normal cells to cancer. The mechanism for evolutionary base substitutions is a time-dependent Topal-Fresco process in which the required unusual tautomers are provided by proton exchange tunneling (see, W.G. Cooper, 1992a). The very good agreement between incidence of cancer data and the model is consistent with the hypothesis that duplex DNA has been evolutionarily designed to supplying an optimum rate of point mutation variation for purposes of (a) providing the species with the ability to respond favorably to changing environmental conditions and (b) to protect the species from adverse consequences of accumulating excessive mutations. (e.g., W.G. Cooper, 1992b). As a result of identifying "tunneling sensitive" DNA codes, consequences of evolutionary lesions in diploid and haploid human genomes are evaluated. The "faster evolving" oocyte genome may be responsible for most evolutionary traits, whereas evolutionarily conserved domains may be supplied by the "slower evolving" male haploid genome. Evidence from fragile X genetic systems support this conclusion. The model further illustrates how fragile X genetic properties could be a result of evolutionary lesions altering genetic specificities of "tunneling sensitive" CGG codes to specify DNA synthesis initiation codons, CUG or UUG. This could cause reinitiation of DNA synthesis and the addition of more CGG codes to the "tunneling sensitive" segment of consecutive (CGG)n repeats which would explain how (CGG)n segments are "expanded" during oogenesis.

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