Alterations in DNA repair efficiency are involved in the radioresistance of esophageal adenocarcinoma

Radiat Res. 2010 Dec;174(6):703-11. doi: 10.1667/RR2295.1. Epub 2010 Oct 4.


To study radioresistance in esophageal adenocarcinoma, we generated an isogenic cell line model by exposing OE33 esophageal adenocarcinoma cells to clinically relevant fractionated doses of radiation (cumulative dose 50 Gy). A clonogenic assay confirmed enhanced survival of the radioresistant OE33 subline (OE33 R). To our knowledge, we are the first to generate an isogenic model of radioresistance in esophageal adenocarcinoma. This model system was characterized in terms of growth, cell cycle distribution and checkpoint operation, apoptosis, reactive oxygen species generation and scavenging, and DNA damage. While similar properties were found for both the parental OE33 (OE33 P) cells and radioresistant OE33 R cells, OE33 R cells demonstrated greater repair of radiation-induced DNA damage. Our results suggest that the radioresistance of OE33 R cells is due at least in part to increased DNA repair.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenocarcinoma / genetics
  • Adenocarcinoma / pathology
  • Adenocarcinoma / radiotherapy*
  • Apoptosis / radiation effects
  • Cell Cycle / radiation effects
  • Cell Line, Tumor
  • Cell Proliferation / radiation effects
  • DNA Repair*
  • Esophageal Neoplasms / genetics
  • Esophageal Neoplasms / pathology
  • Esophageal Neoplasms / radiotherapy*
  • Histones / analysis
  • Humans
  • Radiation Tolerance*
  • Reactive Oxygen Species / metabolism


  • H2AX protein, human
  • Histones
  • Reactive Oxygen Species