| Literature DB >> 17097223 |
Frank Schönleben1, Wanglong Qiu, Karl C Bruckman, Nancy T Ciau, Xiaojun Li, Margaret H Lauerman, Harold Frucht, John A Chabot, John D Allendorf, Helen E Remotti, Gloria H Su.
Abstract
The Raf/MEK/ERK (MAPK) signal transduction is an important mediator of a number of cellular fates including growth, proliferation, and survival. The BRAF gene is activated by oncogenic RAS, leading to cooperative effects in cells responding to growth factor signals. Our study was performed to elucidate a possible role of BRAF in the development of IPMN (Intraductal Papillary Mucinous Neoplasm) and IPMC (Intraductal Papillary Mucinous Carcinoma) of the pancreas. Mutations of BRAF and KRAS were evaluated in 36 IPMN/IPMC samples and two mucinous cystadenomas by direct genomic sequencing. Exons 1 for KRAS, and 5, 11, and 15 for BRAF were examined. Totally we identified 17 (47%) KRAS mutations in exon 1, codon 12 and one missense mutation (2.7%) within exon 15 of BRAF. The mutations appear to be somatic since the same alterations were not detected in the corresponding normal tissues. Our data provide evidence that oncogenic properties of BRAF contribute to the tumorigenesis of IPMN/IPMC, but at a lower frequency than KRAS.Entities:
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Year: 2006 PMID： 17097223 PMCID： PMC1865507 DOI： 10.1016/j.canlet.2006.09.007
Source DB: PubMed Journal: Cancer Lett ISSN： 0304-3835 Impact factor: 8.679