ROLES OF EVOLUTION, QUANTUM-MECHANICS AND POINT MUTATIONS IN ORIGINS OF CANCER

The fact point genetic lesions-which provide the species with an abili ty 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 addit ional function for evolutionary processes. In particular, this suggest s 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 th e adverse consequences of accumulating mutations beyond an unsafe uppe r limit. This hypothesis is used to construct a mutation model polynom ial for incidence of human cancer as a function of age. The model assu mes that point lesion sensitive proto-oncogenes and ''p53-type'' genes are evolutionarily conserved and must exhibit wild-type genetic infor mation at fertilization for proper growth. Subsequently, evolutionary lesions populate these conserved domains, eventually causing point les ion sensitive genes to yield amino acid substituted proteins capable o f participation in transforming normal cells to cancer. The mechanism for evolutionary base substitutions is a time-dependent Topal-Fresco p rocess 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 supplyi ng an optimum rate of point mutation variation for purposes of (a) pro viding the species with the ability to respond favorably to changing e nvironmental conditions and (b) to protect the species from adverse co nsequences of accumulating excessive mutations. (e.g., W.G. Cooper, 19 92b). As a result of identifying ''tunneling sensitive'' DNA codes, co nsequences of evolutionary lesions in diploid and haploid human genome s are evaluated. The ''faster evolving'' oocyte genome may be responsi ble for most evolutionary traits, whereas evolutionarily conserved dom ains may be supplied by the ''slower evolving'' male haploid genome. E vidence from fragile X genetic systems support this conclusion. The mo del further illustrates how fragile X genetic properties could be a re sult of evolutionary lesions altering genetic specificities of ''tunne ling sensitive'' CGG codes to specify DNA synthesis initiation codons, CUG or UUG. This could cause reinitiation of DNA synthesis and the ad dition of more CGG codes to the ''tunneling sensitive'' segment of con secutive (CGG)n repeats which would explain how (CGG)n segments are '' expanded'' during oogenesis.