Skip to Content

As a result of the current Federal government funding situation, the information on this website may not be up to date or acted upon.

The NIH Clinical Center (the research hospital of NIH) is open. For more details about its operating status, please visit

Updates regarding government operating status and resumption of normal operations can be found at

Discovering the causes of cancer and the means of prevention

Publications Search - Abstract View

Title: Allelotyping of esophageal squamous-cell carcinoma on chromosome 13 defines deletions related to family history.
Authors: Hu N,  Su H,  Li WJ,  Giffen C,  Goldstein AM,  Hu Y,  Wang C,  Roth MJ,  Li G,  Dawsey SM,  Xu Y,  Taylor PR,  Emmert-Buck MR
Journal: Genes Chromosomes Cancer
Date: 2005 Nov
Branches: ITEB, MEB
PubMed ID: 16015646
PMC ID: not available
Abstract: We previously reported that esophageal squamous-cell cancers (ESCC) from Shanxi Province in China show frequent allelic loss on chromosome 13. Moreover, tumors from patients with a positive family history of upper gastrointestinal tumors exhibit more frequent loss of heterozygosity (LOH) on this chromosome than do those from patients without a family history. These results suggest the possibility of a familial ESCC susceptibility gene. To investigate this phenomenon further, we performed an in-depth analysis of allelic-loss data sets from both patients with and without a family history of upper gastrointestinal tumors. Comparisons between deletion frequency and location were made with respect to family history status, risk factors, and clinical/pathologic characteristics of the tumors. The analysis confirmed that tumor LOH was significantly higher in patients with a positive family history than in those who were family-history-negative, and four common deletion regions in these family-history-positive patients were defined. Statistically significant associations were also observed between allelic loss and tumor grade and location, as well as the presence of lymph node metastases. Taken together, these data indicate that a gene or genes on chromosome 13 play an important role in the etiology and progression of ESCC.