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作 者:PeterLy UgurEskiocak Chelsea RParker Kenneth JHarris Woodring EWright Jerry WShay
出 处:《Cell Research》2012年第11期1605-1608,共4页细胞研究(英文版)
摘 要:Dear Editor, Genomic sequencing of human tumor-derived DNA has identified a vast number of novel tissue-specific genetic mutations occurring at varying frequencies [1]. Frequently mutated genes are informally referred to as driver alterations (or candidate cancer genes, CAN- genes), whereas those less frequently mutated are con- sidered passenger alterations [ 1, 2]. With few exceptions, the majority of mutations are loss-of-function alterations and the ones that occur rarely are presumed to be a by- product of genomic instability or normal mutation rates that do not directly contribute to tumor progression (pas- sengers) [3]. In addition to computational and biostatisti- cal models for parsing driver from passenger mutations, the utility of biological assays to functionally interrogate cancer genomes is required to determine which of these mutations are able to contribute to a particular tumori- genic phenotype (i.e., anchorage-independent growth, resistance to apoptosis, enhanced invasion through extra- cellular matrices).
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