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• W2011066075 abstract "Cancer is a consequence of the accumulation of mutations and epigenetic alterations in oncogenes and tumor-suppressor genes. Recent advances in high-throughput sequencing methods and methylation array technology has led to genome-wide analyses of gene alterations in a wide variety of cancers, including colorectal cancer (1). These studies have revealed that there are hundreds to thousands of DNA alterations in the average colorectal cancer genome, and that there are roughly 80–100 genes that are commonly altered by nonsynonymous mutations and roughly 15 mutations in candidate “driver” genes per genome. (“Driver genes” are those genes that induce the formation of cancer.) These studies have also revealed considerable heterogeneity between colorectal cancers and that the majority of gene mutations are likely passenger events, which are bystanders in cancer formation. Thus, one of the major challenges facing cancer biologists now is how to identify the mutated genes that are functionally relevant in the tumorigenesis process. The traditional approach to deciphering which genes are functionally relevant assumes mutations in genes will lead to constitutive tumor-promoting or tumor-suppressing biological effects. Thus, mutations in genes for the tyrosine kinases (e.g., EGFR, BRAF, and so forth) have typically been classified as oncogenic because they often induce a constant state of inappropriate proliferation, whereas other genes, such as BRCA2, are most often classified as tumor-suppressor genes because these mutations impair DNA fidelity." @default.
• W2011066075 created "2016-06-24" @default.
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• W2011066075 date "2013-02-08" @default.
• W2011066075 modified "2023-09-30" @default.
• W2011066075 title "Context is everything for dependence receptors in colorectal cancer" @default.
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• W2011066075 doi "https://doi.org/10.1073/pnas.1300758110" @default.
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