Loss of TGFβ signaling increases alternative end-joining DNA repair that sensitizes to genotoxic therapies across cancer types

Author:

Liu Qi1ORCID,Palomero Luis2ORCID,Moore Jade1ORCID,Guix Ines1,Espín Roderic2ORCID,Aytés Alvaro2,Mao Jian-Hua3ORCID,Paulovich Amanda G.4ORCID,Whiteaker Jeffrey R.4ORCID,Ivey Richard G.4ORCID,Iliakis George5ORCID,Luo Daxian5,Chalmers Anthony J.6ORCID,Murnane John1,Pujana Miquel Angel2ORCID,Barcellos-Hoff Mary Helen1ORCID

Affiliation:

1. Department of Radiation Oncology and Helen Diller Family Comprehensive Cancer Center, University of California San Francisco, San Francisco, CA 94143, USA.

2. ProCURE, Catalan Institute of Oncology, Oncobell, Bellvitge Institute for Biomedical Research (IDIBELL), L’Hospitalet del Llobregat, Barcelona 08908, Catalonia, Spain.

3. Biological Systems and Engineering Division, Berkeley Biomedical Data Science Center, Lawrence Berkeley National Laboratory, Berkeley, CA 94720, USA.

4. Clinical Research Division, Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA.

5. Institute of Medical Radiation Biology, University of Duisburg-Essen, University Hospital Essen, Essen 45147, Germany.

6. Institute of Cancer Sciences and Beatson West of Scotland Cancer Centre, University of Glasgow, Glasgow G12 8QQ, Scotland, UK.

Abstract

The impact of TGFβ signaling on DNA repair competency is observed in a pan-cancer analysis of survival after treatments that cause DNA damage.

Funder

National Cancer Institute

European Regional Development Fund

German Federal Ministry of Education and Research

Publisher

American Association for the Advancement of Science (AAAS)

Subject

General Medicine

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