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4 October 2010 Alterations in DNA Repair Efficiency are Involved in the Radioresistance of Esophageal Adenocarcinoma
Niamh Lynam-Lennon, John V. Reynolds, Graham P. Pidgeon, Joanne Lysaght, Laure Marignol, Stephen G. Maher
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Abstract

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.

Niamh Lynam-Lennon, John V. Reynolds, Graham P. Pidgeon, Joanne Lysaght, Laure Marignol, and Stephen G. Maher "Alterations in DNA Repair Efficiency are Involved in the Radioresistance of Esophageal Adenocarcinoma," Radiation Research 174(6a), 703-711, (4 October 2010). https://doi.org/10.1667/RR2295.1
Received: 11 May 2010; Accepted: 1 August 2010; Published: 4 October 2010
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