Biology 2581B Lecture Notes - Lecture 13: Punctuated Equilibrium, Kras, P53

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Applications of basic evolutionary theory to populations for tumor cells. Think of a population of tumor cells as a regulator population. If some type of variation arises, if that variation is favored by selection it will tend to increase in frequency. As tumor cells grow, they suffer more mutations in various combinations of genes. Driver mutations: pushing cells towards excess proliferation. Or maybe there"s a catastrophic event that creates several mutations at the same time (not sequential) = punctuated evolution. Most successful cells may break free from original tumor and travel to other parts of the body where they encounter yet again diverse environments, diverse selection pressures. Mutation in kras drives proliferation gain of function. Loss of function in tp53 also causes cancer. Deregulation of oncogenes or tumor-suppressor genes results in excessive cell proliferation. Oncogenes: upregulated gene would be dominant heterozygous change: dominant-acting mutation; mutation in either allele.

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