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Comparative genomic hybridization of esophageal and gastroesophageal adenocarcinomas shows consensus areas of DNA gain and loss
Author(s) -
Moskaluk Christopher A.,
Hu Jie,
Perlman Elizabeth J.
Publication year - 1998
Publication title -
genes, chromosomes and cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.754
H-Index - 119
eISSN - 1098-2264
pISSN - 1045-2257
DOI - 10.1002/(sici)1098-2264(199808)22:4<305::aid-gcc6>3.0.co;2-z
Subject(s) - comparative genomic hybridization , biology , chromosome , gene , cancer , cancer research , gene duplication , esophageal cancer , suppressor , genetics
Relatively little is known about the genetic changes that occur in esophageal and gastroesophageal adenocarcinomas. To provide a survey of relative DNA gains and losses in these cancers, we microdissected 15 primary human esophageal and gastroesophageal adenocarcinomas to enrich for cancer cells and subsequently performed comparative genomic hybridization. Eighteen regions of high‐level amplification were detected in 11 tumors, with 8p23, 17q21, and 18p11 showing four, three, and two such events, respectively. The most common minimal regions of gain were 8q24 (8/15), 20q (7/15), 17q21 (7/15), and 7p11–15 (7/15 ). The most common minimal regions of loss were 5q12–21 (8/15), 4q10–24 (5/15), 4p (5/15), and 18q (3/15). These results implicate the well‐characterized oncogenes MYC (8q24) and ERBB2 (17q21), and they predict the involvement of additional oncogenes on 8p23, 20q, and chromosome 7 in the pathogenesis of these cancers. Chromosomes 4 and 5 are frequent targets of deletion in these tumors and may harbor novel tumor suppressor genes. Genes Chromosomes Cancer 22:305–311, 1998. © 1998 Wiley‐Liss, Inc.