| Literature DB >> 12545169 |
Suna Wang1, Yuriko Mori, Fumiaki Sato, Jing Yin, Yan Xu, Tong-Tong Zou, Andreea Olaru, Martha C Kimos, Kellie Perry, Florin M Selaru, Elena Deacu, Menghong Sun, Ying-Chang Shi, David Shibata, John M Abraham, Bruce D Greenwald, Stephen J Meltzer.
Abstract
Frequent loss of heterozygosity (LOH) on human chromosome 7q31 has been reported in numerous malignancies. Suppressor of tumorigenicity 7 (ST7) has been identified as a candidate tumor suppressor gene in this region. To identify whether 7q31 and genetic alterations of ST7 were involved in human esophageal carcinogenesis, we performed LOH mapping of a 5.4 cM region at 7q31-q35 in 43 primary esophageal carcinomas, as well as mutational analyses of the ST7 gene in tumors with LOH in this region. Of 43 tumors, 12 (28%) showed LOH at 7q31-q35. These included four (22%) of 18 squamous cell carcinomas and eight (32%) of 25 adenocarcinomas. The peak LOH locus was D7S480, lying 4.2 Mb telomeric to ST7 and showing LOH in eight of 37 informative tumors, or 22%. No mutations were found in the entire coding or flanking intronic regions of the ST7 gene among 12 tumors with 7q-LOH. In addition, quantitative RT-PCR analyses of ST7 mRNA expression levels in 11/13 normal-tumor pairs failed to show more than a 50% decrease in tumor ST7 mRNA relative to matched normal tissues. These data suggest that LOH at 7q31-q35 is involved in the origin or progression of at least a subset of esophageal carcinomas, but that ST7 is not the target gene of this somatic event.Entities:
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Year: 2003 PMID: 12545169 DOI: 10.1038/sj.onc.1206125
Source DB: PubMed Journal: Oncogene ISSN: 0950-9232 Impact factor: 9.867