中文摘要：

许多人的肿瘤房间被表皮的生长因素受体(EGFR ) 的 overexpression 或变化描绘。新兴的证据在 transcriptional 规定显示那 EGFR，以及一些它的下游的部件，到原子核的罐头 translocate 和戏角色，表明 DNA 双海滨裂缝(DSB ) 的传导和修理。在它的原子表明的 EGFR 由包括 DNA-PK， ATM， Rad51 和 BRCA1 与蛋白质交往支持 DSB 修理，在 DSB 包含了修理，经由 PI3K-Akt 和 Ras-Raf-MAPK 小径。在肿瘤房间的 DNA 损坏修理在放射疗法和化疗作为一个吸引人的目标正在出现。它的下游的部件的 EGFR 功能的打断，或那些，为在肿瘤房间使 DNA 损坏修理惊讶介绍有希望的策略。

英文摘要：

Many human tumor cells are characterized by overexpression or mutation of epidermal growth factor receptor （EGFR）. Emerging evidence indicates that EGFR, as well as some of its downstream components, can translocate to the nucleus and play roles in transcriptional regulation, signaling conduction and repair of DNA double strands breaks （DSBs）. EGFR in its nuclear manifesta- tion promotes DSB repair by interacting with proteins including DNA-PK, ATM, Rad51 and BRCA1, involved in DSB repair, via the PI3K-Akt and Ras-Raf-MAPK pathways. DNA damage repair in tumor cells is emerging as an attractive target in radiotherapy and chemotherapy. Interruption of EGFR functions, or those of its downstream components, presents a promising strategy for confounding DNA damage repair in tumor cells.