An LOH and mutational investigation of the ST7 gene locus in human esophageal carcinoma

Suna Wang, 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

Research output: Contribution to journalArticlepeer-review

10 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)467-470
Number of pages4
Issue number3
StatePublished - Jan 23 2003
Externally publishedYes


  • 7q31
  • Esophageal cancer
  • Expression
  • LOH
  • Mutation
  • ST7

ASJC Scopus subject areas

  • Molecular Biology
  • Genetics
  • Cancer Research


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