Homologous-recombination-deficient tumours are dependent on Polθ-mediated repair

Raphael Ceccaldi, Jessica C. Liu, Ravindra Amunugama, Ildiko Hajdu, Benjamin Primack, Mark I. R. Petalcorin, Kevin W. O’Connor, Panagiotis A. Konstantinopoulos, Stephen J. Elledge, Simon J. Boulton, Timur Yusufzai and Alan D. D’Andrea ()
Additional contact information
Raphael Ceccaldi: Dana-Farber Cancer Institute, Harvard Medical School
Jessica C. Liu: Dana-Farber Cancer Institute, Harvard Medical School
Ravindra Amunugama: Howard Hughes Medical Institute, Harvard Medical School
Ildiko Hajdu: Howard Hughes Medical Institute, Brigham and Women’s Hospital
Benjamin Primack: Dana-Farber Cancer Institute, Harvard Medical School
Mark I. R. Petalcorin: DNA Damage Response Laboratory, Cancer Research UK, London Research Institute, Clare Hall, South Mimms EN6 3LD, UK
Kevin W. O’Connor: Dana-Farber Cancer Institute, Harvard Medical School
Panagiotis A. Konstantinopoulos: Medical Gynecologic Oncology Program, Dana-Farber Cancer Institute, Harvard Medical School
Stephen J. Elledge: Howard Hughes Medical Institute, Brigham and Women’s Hospital
Simon J. Boulton: DNA Damage Response Laboratory, Cancer Research UK, London Research Institute, Clare Hall, South Mimms EN6 3LD, UK
Timur Yusufzai: Dana-Farber Cancer Institute, Harvard Medical School
Alan D. D’Andrea: Dana-Farber Cancer Institute, Harvard Medical School

Nature, 2015, vol. 518, issue 7538, 258-262

Abstract: In studies in mammalian cells, polymerase theta (Polθ, also known as POLQ) is identified as the polymerase responsible for non-homologous end joining DNA repair; this DNA repair pathway acts in many tumours when homologous recombination is inactivated and the identification of the polymerase responsible may aid the development of new therapeutic approaches.

Date: 2015
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DOI: 10.1038/nature14184

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