Molecular pathogenesis of adenocarcinomas in barrett’s esophagus: Role of the tumor suppressor gene p53

P. M. Schneider, A. G. Casson, A. H. Hölscher, S. Schweighart, S. Mizumoto, J. R. Siewert, J. A. Roth

Research output: Contribution to journalArticlepeer-review

Abstract

Mutations in the p53 tumor suppressor gene are involved in the molecular pathogenesis of adenocarcinomas in Barrett’s esophagus in approximately 50% of patients. They occur at an early stage of tumor development presumably prior to the development of invasive cancer in premalignant Barrett’s epithelium. The majority of mutations are transition-type mutations, which is in striking contrast to esophageal squamous cell carcinomas and favors a different molecular pathogenesis for the two types of esophageal cancer. A prospective long-term study in a substantial number of patients with benign Barrett’s esophagus is mandatory to finally elucidate the role of p53 mutations as a marker for the malignant potential of Barrett’s epithelium.

Original languageEnglish (US)
Pages (from-to)36-40
Number of pages5
JournalOncology research and treatment
Volume20
Issue number1
DOIs
StatePublished - Jan 1 1997

ASJC Scopus subject areas

  • Hematology
  • Oncology
  • Cancer Research

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