A Comparative Genomic Approach for Identifying Synthetic Lethal Interactions in Human Cancer

被引：53

作者：

Deshpande, Raamesh ^{[1
]}

Asiedu, Michael K. ^{[3
]}

Klebig, Mitchell ^{[3
,4
]}

Sutor, Shari ^{[3
]}

Kuzmin, Elena ^{[5
]}

Nelson, Justin ^{[2
]}

Piotrowski, Jeff ^{[7
]}

Shin, Seung Ho ^{[2
]}

Yoshida, Minoru ^{[6
]}

Costanzo, Michael ^{[5
]}

Boone, Charles ^{[5
,6
]}

Wigle, Dennis A. ^{[2
,3
]}

Myers, Chad L. ^{[1
,2
]}

机构：

[1] Univ Minnesota, Dept Comp Sci & Engn, Minneapolis, MN USA

[2] Univ Minnesota, Program Biomed Informat & Computat Biol, Minneapolis, MN USA

[3] Mayo Clin, Dept Surg, Rochester, MN USA

[4] Mayo Clin, Dept Lab Med & Pathol, Mol Genet Lab, Rochester, MN USA

[5] Univ Toronto, Terrence Donnelly Ctr Cellular & Biomol Res, Dept Mol Genet, Toronto, ON M5S 1A1, Canada

[6] RIKEN, Adv Sci Inst, Chem Genom Res Grp, Saitama, Japan

[7] Univ Wisconsin, Great Lakes Bioenergy Res Ctr, Madison, WI USA

来源：

CANCER RESEARCH | 2013年 / 73卷 / 20期

基金：

美国国家科学基金会; 加拿大健康研究院;

关键词：

SOFT-PART SARCOMA; POLY(ADP-RIBOSE) POLYMERASE; RNA INTERFERENCE; OVARIAN-CANCER; CELL-LINES; TUMORS; GENE; VULNERABILITIES; DISCOVERY; REVEALS;

D O I：

10.1158/0008-5472.CAN-12-3956

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Synthetic lethal interactions enable a novel approach for discovering specific genetic vulnerabilities in cancer cells that can be exploited for the development of therapeutics. Despite successes in model organisms such as yeast, discovering synthetic lethal interactions on a large scale in human cells remains a significant challenge. We describe a comparative genomic strategy for identifying cancer-relevant synthetic lethal interactions whereby candidate interactions are prioritized on the basis of genetic interaction data available in yeast, followed by targeted testing of candidate interactions in human cell lines. As a proof of principle, we describe two novel synthetic lethal interactions in human cells discovered by this approach, one between the tumor suppressor gene SMARCB1 and PSMA4, and another between alveolar soft-part sarcoma-associated ASPSCR1 and PSMC2. These results suggest therapeutic targets for cancers harboring mutations in SMARCB1 or ASPSCR1 and highlight the potential of a targeted, cross-species strategy for identifying synthetic lethal interactions relevant to human cancer. Cancer Res; 73(20); 6128-36. (C) 2013 AACR.

引用

页码：6128 / 6136

页数：9

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