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

被引：0

作者：

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

Alan D. D’Andrea

机构：

[1] Dana-Farber Cancer Institute,Department of Radiation Oncology

[2] Harvard Medical School,Department of Biological Chemistry & Molecular Pharmacology

[3] Harvard Medical School,Department of Molecular & Cellular Biology

[4] Harvard University,Department of Biological Chemistry and Molecular Pharmacology

[5] Howard Hughes Medical Institute,Division of Genetics

[6] Harvard Medical School,Department of Medical Oncology

[7] Howard Hughes Medical Institute,undefined

[8] Brigham and Women’s Hospital,undefined

[9] DNA Damage Response Laboratory,undefined

[10] Cancer Research UK,undefined

[11] London Research Institute,undefined

[12] Clare Hall,undefined

[13] South Mimms EN6 3LD,undefined

[14] UK,undefined

[15] Medical Gynecologic Oncology Program,undefined

[16] Dana-Farber Cancer Institute,undefined

[17] Harvard Medical School,undefined

来源：

Nature | 2015年 / 518卷

关键词：

D O I：

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学科分类号：

摘要：

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.

引用

页码：258 / 262

页数：4

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