53BP1 loss rescues BRCA1 deficiency and is associated with triple-negative and BRCA-mutated breast cancers

被引：0

作者：

Peter Bouwman

Amal Aly

Jose M Escandell

Mark Pieterse

Jirina Bartkova

Hanneke van der Gulden

Sanne Hiddingh

Maria Thanasoula

Atul Kulkarni

Qifeng Yang

Bruce G Haffty

Johanna Tommiska

Carl Blomqvist

Ronny Drapkin

David J Adams

Heli Nevanlinna

Jiri Bartek

Madalena Tarsounas

Shridar Ganesan

Jos Jonkers

机构：

[1] The Netherlands Cancer Institute,Division of Molecular Biology

[2] Cancer Institute of New Jersey,Department of Obstetrics and Gynecology

[3] Telomere and Genome Stability Group,Department of Oncology

[4] The Cancer Research UK-MRC Gray Institute for Radiation Oncology and Biology,Department of Medical Oncology

[5] Institute of Cancer Biology and Centre for Genotoxic Stress Research,undefined

[6] Danish Cancer Society,undefined

[7] Helsinki University Central Hospital,undefined

[8] Helsinki University Central Hospital,undefined

[9] Center of Molecular Oncologic Pathology,undefined

[10] Dana-Farber Cancer Institute,undefined

[11] Wellcome Trust Sanger Institute,undefined

[12] Wellcome Trust Genome Campus Hinxton,undefined

[13] Institute of Molecular and Translational Medicine,undefined

[14] Palacky University,undefined

来源：

Nature Structural & Molecular Biology | 2010年 / 17卷

关键词：

D O I：

暂无

中图分类号：

学科分类号：

摘要：

A transposon mutagenesis screen indicates that loss of 53BP1 expression rescues the clonal growth defect of BRCA1 null cells. 53BP1 deficiency is shown to abrogate the cell cycle arrest triggered in the absence of BRCA1 and to partially restore homologous recombination. The potential clinical implications of these findings are supported by the reduction of 53BP1 expression in sporadic triple-negative and BRCA-associated breast cancers.

引用

页码：688 / 695

页数：7

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