[Multiple tumor suppressor 1/p16 gene alterations in human esophageal squamous-cell carcinoma: clinical significance and regional difference]

Zhonghua Zhong Liu Za Zhi. 1999 Sep;21(5):359-62.
[Article in Chinese]

Abstract

Objective: To further understand multiple tumor suppressor 1/p16 (mts1/p16) gene alterations in squamous-cell esophageal carcinoma (EC) in relation to its biologic behavior and regional difference.

Methods: Samples of human EC from 92 patients residing in Zhejiang province and in Linxian, Henan province were analyzed for the expression, mutation and deletion of the multiple tumor suppressor gene (mts1/p16) by immunohistochemical staining, polymerase chain reaction and single strand conformation polymorphism.

Results: mts1/p16 expression at protein level was demonstrated in 44 cases (47.8%). Gene deletion was detected in 22 cases (23.9%) and point mutation in 5 cases (5.4%). Expression of mst1/p16 showed significant correlation with pathologic staging, lymph node status and survival. However, deletion of mst1/p16 did not show correlation with the clinico-pathologic parameters. EC patients in stage T2 from Linxian had significantly lower rate of mst1/p16 protein expression compared to those from Zhejiang province at the same time period. Moreover, there was close association between gene alterations (mutation + deletion) and frequency of lymph node metastasis in Zhejiang EC patients. No such association was observed in EC patients from Linxian.

Conclusion: msts1/p16 gene alteration is a common genetic event in the carcinogenesis and progression of human esophageal cancer. EC patients from two different regions present differential alterations in mst1/p16 gene.

Publication types

  • English Abstract
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Carcinoma, Squamous Cell / genetics*
  • Carcinoma, Squamous Cell / mortality
  • Carcinoma, Squamous Cell / pathology
  • Esophageal Neoplasms / genetics*
  • Esophageal Neoplasms / mortality
  • Esophageal Neoplasms / pathology
  • Gene Deletion
  • Genes, p16*
  • Humans
  • Mutation