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    Online-Ressource
    Online-Ressource
    American Association for Cancer Research (AACR) ; 2014
    In:  Cancer Research Vol. 74, No. 19_Supplement ( 2014-10-01), p. 2202-2202
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 74, No. 19_Supplement ( 2014-10-01), p. 2202-2202
    Kurzfassung: Colorectal cancer is a heterogeneous disorder than arises via multiple distinct pathways, from tubular adenomas (TAs) and serrated polyps (SPs), which are clinically, morphologically, and molecularly different. We examined PIK3CA amplification in colorectal precancerous legions, including TAs and SPs. DNA was isolated from paired normal and tumoral tissues in 64 TAs and 32 SPs. PIK3CA amplification, KRAS mutation, and BRAF mutation were analyzed by real-time PCR. PIK3CA amplification was found in 25% of TAs and 9.4% of SPs, respectively and low and high grade of TAs showed similar frequency of PIK3CA amplification. KRAS and BRAF mutations were mutually exclusive in both TAs and SPs. In TAs, PIK3CA amplification was associated with distal colon and it was mutually exclusive with KRAS mutation. These results suggest that PIK3CA amplification may be early and important event in colorectal carcinogenesis and may drive the development of TAs independently with KRAS mutation. Keyword: colorectal cancer, PIK3CA amplification, serrated polyps, tubular adenomas Note: This abstract was not presented at the meeting. Citation Format: Jae-Ho Lee, Dae-Kwang Kim, In-Jang Choi, IlSeon Hwang, Yu-Na Kang, Shin Kim. PIK3CA amplification was not associated with serrated polyps but tubular adenomas in colorectal lesions. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 2202. doi:10.1158/1538-7445.AM2014-2202
    Materialart: Online-Ressource
    ISSN: 0008-5472 , 1538-7445
    RVK:
    RVK:
    Sprache: Englisch
    Verlag: American Association for Cancer Research (AACR)
    Publikationsdatum: 2014
    ZDB Id: 2036785-5
    ZDB Id: 1432-1
    ZDB Id: 410466-3
    Standort Signatur Einschränkungen Verfügbarkeit
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