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OB Drivers of colorectal cancers the design of targeted therapeutics for human colorectal cancers (crc) is dependent on the ability to distinguish alterations that are causal in tumor formation and progression from those that have little or no effect on tumor growth. to identify novel drivers of crc...

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Veröffentlicht in:Nature genetics 2009-04, Vol.41 (4), p.390
Hauptverfasser: Axton, Myles, Bahcall, Orli, Khidr, Lily, Vogan, Kyle
Format: Artikel
Sprache:eng
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Zusammenfassung:OB Drivers of colorectal cancers the design of targeted therapeutics for human colorectal cancers (crc) is dependent on the ability to distinguish alterations that are causal in tumor formation and progression from those that have little or no effect on tumor growth. to identify novel drivers of crc, David largaespada and colleagues (Science published online, doi:10.1126/science.1163040; 26 February 2009) catalogued genes with common insertion sites (cis) generated in tumors harvested from a gastrointestinal (gi) tract-specific transgenic mouse model that exploits the transposition of a mutagen catalyzed by sleeping Beauty (sB) transposase. comparison of mouse cis genes with human genes that are mutated, amplified, deleted or aberrantly expressed in crc, listed in the catalog of somatic Mutations in cancer database (cOsMic), or known cancer genes identified by the cancer genome Project, revealed a significant overlap of mouse candidate genes and human genes that are altered in cancer. the authors identified 15 cis genes that are most likely to cause crc by virtue of being classified in at least three out of the five aforementioned categories.
ISSN:1061-4036
1546-1718