| Literature DB >> 28753431 |
E Robert McDonald1, Antoine de Weck2, Michael R Schlabach2, Eric Billy2, Konstantinos J Mavrakis2, Gregory R Hoffman2, Dhiren Belur2, Deborah Castelletti2, Elizabeth Frias2, Kalyani Gampa2, Javad Golji2, Iris Kao2, Li Li2, Philippe Megel2, Thomas A Perkins2, Nadire Ramadan2, David A Ruddy2, Serena J Silver2, Sosathya Sovath2, Mark Stump2, Odile Weber2, Roland Widmer2, Jianjun Yu2, Kristine Yu2, Yingzi Yue2, Dorothee Abramowski2, Elizabeth Ackley2, Rosemary Barrett2, Joel Berger2, Julie L Bernard2, Rebecca Billig2, Saskia M Brachmann2, Frank Buxton2, Roger Caothien2, Justina X Caushi2, Franklin S Chung2, Marta Cortés-Cros2, Rosalie S deBeaumont2, Clara Delaunay2, Aurore Desplat2, William Duong2, Donald A Dwoske2, Richard S Eldridge2, Ali Farsidjani2, Fei Feng2, JiaJia Feng2, Daisy Flemming2, William Forrester2, Giorgio G Galli2, Zhenhai Gao2, François Gauter2, Veronica Gibaja2, Kristy Haas2, Marc Hattenberger2, Tami Hood2, Kristen E Hurov2, Zainab Jagani2, Mathias Jenal2, Jennifer A Johnson2, Michael D Jones2, Avnish Kapoor2, Joshua Korn2, Jilin Liu2, Qiumei Liu2, Shumei Liu2, Yue Liu2, Alice T Loo2, Kaitlin J Macchi2, Typhaine Martin2, Gregory McAllister2, Amandine Meyer2, Sandra Mollé2, Raymond A Pagliarini2, Tanushree Phadke2, Brian Repko2, Tanja Schouwey2, Frances Shanahan2, Qiong Shen2, Christelle Stamm2, Christine Stephan2, Volker M Stucke2, Ralph Tiedt2, Malini Varadarajan2, Kavitha Venkatesan2, Alberto C Vitari2, Marco Wallroth2, Jan Weiler2, Jing Zhang2, Craig Mickanin2, Vic E Myer2, Jeffery A Porter2, Albert Lai2, Hans Bitter2, Emma Lees2, Nicholas Keen2, Audrey Kauffmann2, Frank Stegmeier2, Francesco Hofmann2, Tobias Schmelzle3, William R Sellers2.
Abstract
Elucidation of the mutational landscape of human cancer has progressed rapidly and been accompanied by the development of therapeutics targeting mutant oncogenes. However, a comprehensive mapping of cancer dependencies has lagged behind and the discovery of therapeutic targets for counteracting tumor suppressor gene loss is needed. To identify vulnerabilities relevant to specific cancer subtypes, we conducted a large-scale RNAi screen in which viability effects of mRNA knockdown were assessed for 7,837 genes using an average of 20 shRNAs per gene in 398 cancer cell lines. We describe findings of this screen, outlining the classes of cancer dependency genes and their relationships to genetic, expression, and lineage features. In addition, we describe robust gene-interaction networks recapitulating both protein complexes and functional cooperation among complexes and pathways. This dataset along with a web portal is provided to the community to assist in the discovery and translation of new therapeutic approaches for cancer.Entities:
Keywords: CCLE; DRIVE; RNA interference; cancer dependency; functional genomics; synthetic lethality
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Year: 2017 PMID： 28753431 DOI： 10.1016/j.cell.2017.07.005
Source DB: PubMed Journal: Cell ISSN： 0092-8674 Impact factor: 41.582