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DNA repair after oncological therapy (radiotherapy and chemotherapy) 

DNA repair after oncological therapy (radiotherapy and chemotherapy)
DNA repair after oncological therapy (radiotherapy and chemotherapy)

Ekkehard Dikomey

, Kerstin Borgmann

, Malte Kriegs

, Wael Y. Mansour

, Cordula Petersen

, and Thorsten Rieckmann



We have clarified how EGFR inhibition radiosensitizes tumour cells, which helps explain why recent related clinical trials were unsuccessful.

Recent progress on targeting approaches for HPV-positive tumours has been included.

The paragraph on cell cycle checkpoint targets has been updated.

A few recent references have been added on PARP-1 targeting in tumours with compromised HR or NHEJ function.

Updated on 29 March 2019. The previous version of this content can be found here.
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date: 14 July 2020

The lethal effect of ionizing irradiation on tumour cells is mostly determined by the repair of DNA double-strand breaks (DSBs). Cells are able to repair most of the DSBs, but 1% to 3 % are either non- or mis-repaired, which will then give rise to lethal chromosomal aberrations. Cells have evolved complex DSB repair mechanisms with a stringent hierarchy to guarantee the genomic stability. However, in tumour cells both mechanisms as well as hierarchy are often disturbed. This knowledge is important for an understanding of the radiation response of tumours, but—most of all—for the establishment of new and specific targets for therapy.

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