作者: T.-L. Wang , C. Rago , N. Silliman , J. Ptak , S. Markowitz
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摘要: Although a small fraction of human cancers have increased rates somatic mutation because known deficiencies in DNA repair, little is about the prevalence alterations vast majority cancers. To systematically assess nonsynonymous colorectal neoplasia, we used sequencing to analyze approximately 3.2 Mb coding tumor comprising 1,811 exons from 470 genes. In total, identified only three distinct mutations, two missense changes and one 14-bp deletion, each different gene. The accumulation change per consistent with rate cells that similar normal cells. These data suggest most sporadic do not display mutator phenotype at nucleotide level. They also significant implications for interpretation mutations candidate tumor-suppressor