Mapping of chromosomal imbalances in gastric adenocarcinoma revealed amplified protooncogenesMYCN,MET,WNT2, andERBB2

作者: Michelle Nessling , Sabina Solinas-Toldo , Klaus K. Wilgenbus , Franz Borchard , Peter Lichter

DOI: 10.1002/(SICI)1098-2264(199812)23:4<307::AID-GCC5>3.0.CO;2-#

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摘要: Gastric adenocarcinoma is a malignant tumor with high incidence and low survival rate. In order to identify genetic alterations associated this tumor, we screened 23 gastric adenocarcinomas for recurrent chromosomal imbalances by using comparative genomic hybridization (CGH). The most common gains of material were found on chromosome arms 20q (10 cases), 16p (7 1q (4 cases) 11 cases). Losses observed 4q, 5q, 9p, 21q (3 cases each). Four tumors exhibited high-level amplifications localized regions 2p23-p24, 7q31-q32, 8p21-p22, 10q25-q26, 11q13, 17q11-q21, 20q. Based the position these amplifications, candidate (onco)genes selected subsequently tested Southern blot analysis respective tumors. Of seven candidates, MYCN, MET, WNT2, ERBB2 participate in amplicons samples. four presumably activated oncogenes, two, MYCN previously not assumed play pathogenic role stomach cancer. Among other imbalance, gain seems particularly interesting, because it almost half analyzed highly amplified. Our data allowed us narrow relevant region down commonly gained bands 20q12-q13.1. This imbalanced provide basis searching new putative oncogenes suppressor genes involved development or progression adenocarcinoma.

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