In tumor cells regulation of DNA double strand break repair through EGF receptor involves both NHEJ and HR and is independent of p53 and K-Ras status.

Abstract

The purpose of this study was to examine whether the epidermal growth factor receptor (EGFR) may be used as a general target to modulate DNA double strand break (DSB) repair in tumor cells.

Bibliographical data

Original languageEnglish
Article number1
ISSN0167-8140
Publication statusPublished - 2011
pubmed 21665306