"Our current theory of carcinogenesis is that mutant clones arise through genetic or epigenetic instability, and if they have a reproductive or survival advantage over other cells in the tumor, within their microenvironment, they will expand in the tumor in a selective sweep. Thus, we believe carcinogenesis is characterized by a series of selective sweeps. However, virtually all data on that process to date is cross-sectional, with observations of genetic diversity and large clonal expansions within neoplasms at a single time point ... I will present data that shows that there is genetic and epigenetic diversity within tumors, that clones do expand within tumors, that phenotypes evolve that are associated with increases in the reproduction and survival of those clones, and that therapies select for genetic mutations in tumors that make the clones resistant to the therapies."--Abstract.
""Our current theory of carcinogenesis is that mutant clones arise through genetic or epigenetic instability, and if they have a reproductive or survival advantage over other cells in the tumor, within their microenvironment, they will expand in the tumor in a selective sweep. Thus, we believe carcinogenesis is characterized by a series of selective sweeps. However, virtually all data on that process to date is cross-sectional, with observations of genetic diversity and large clonal expansions within neoplasms at a single time point ... I will present data that shows that there is genetic and epigenetic diversity within tumors, that clones do expand within tumors, that phenotypes evolve that are associated with increases in the reproduction and survival of those clones, and that therapies select for genetic mutations in tumors that make the clones resistant to the therapies."--Abstract."@en
Workshop on Evolution: Foundations, Fundamentals, and Disease (2009 : Hong Kong University of Science and Technology)
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