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. 2016 Apr 1;76(7):1882-91.
doi: 10.1158/0008-5472.CAN-15-2128. Epub 2016 Jan 19.

Ovarian Cancers Harboring Inactivating Mutations in CDK12 Display a Distinct Genomic Instability Pattern Characterized by Large Tandem Duplications (VSports注册入口)

Tatiana Popova  1 , Elodie Manié  2 , Valentina Boeva  3 , Aude Battistella  2 , Oumou Goundiam  4 , Nicholas K Smith  2 , Christopher R Mueller  5 , Virginie Raynal  2 , Odette Mariani  6 , Xavier Sastre-Garau  7 , Marc-Henri Stern  2
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Ovarian Cancers Harboring Inactivating Mutations in CDK12 Display a Distinct Genomic Instability Pattern Characterized by Large Tandem Duplications

Tatiana Popova et al. Cancer Res. .

"V体育平台登录" Abstract

CDK12 is a recurrently mutated gene in serous ovarian carcinoma, whose downregulation is associated with impaired expression of DNA damage repair genes and subsequent hypersensitivity to DNA-damaging agents and PARP1/2 inhibitors. In this study, we investigated the genomic landscape associated with CDK12 inactivation in patients with serous ovarian carcinoma. We show that CDK12 loss was consistently associated with a particular genomic instability pattern characterized by hundreds of tandem duplications of up to 10 megabases (Mb) in size. Tandem duplications were characterized by a bimodal (∼0. 3 and ∼3 Mb) size distribution and overlapping microhomology at the breakpoints. This genomic instability, denoted as the CDK12 TD-plus phenotype, is remarkably distinct from other alteration patterns described in breast and ovarian cancers. The CDK12 TD-plus phenotype was associated with a greater than 10% gain in genomic content and occurred at a 3% to 4% rate in The Cancer Genome Atlas-derived and in-house cohorts of patients with serous ovarian carcinoma. Moreover, CDK12-inactivating mutations together with the TD-plus phenotype were also observed in prostate cancers. Our finding provides new insight toward deciphering the function of CDK12 in genome maintenance and oncogenesis. Cancer Res; 76(7); 1882-91 VSports手机版. ©2016 AACR. .

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