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Synthetic lethality-based targets for discovery of new cancer therapeutics.
Cancer Genomics Proteomics 8, 159-171 (2011)
Synthetic lethality is based on the incompatibility of cell survival with the loss of function of two or more genes, not with loss of function of a single gene. If targets of synthetic lethality are deregulated or mutated in cancer cells, the strategy of synthetic lethality can result in significant increase of therapeutic efficacy and a favourable therapeutic window. In this review, we discuss synthetic lethality based on deficient DNA repair mechanisms, activating mutations of RAS, loss of function mutations of the tumor suppressor genes p53, Rb and von Hippel-Lindau, and disruption of interactive protein kinase networks in the context of development of new anticancer agents.
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Publication type
Article: Journal article
Document type
Review
Keywords
Von--Hippel-Lindau; Negative breast-cancer; Tumor-suppressor gene; Renal-cell Carcinoma; Poly/(ADP-Ribose) Polymerase; Colorecctal-cancer; DNA-repair; C-MYC; Microsatellite instability; Kinase reqirements
ISSN (print) / ISBN
1109-6535
e-ISSN
1790-6245
Journal
Cancer Genomics & Proteomics
Quellenangaben
Volume: 8,
Issue: 4,
Pages: 159-171
Publisher
International Institute of Anticancer Research
Non-patent literature
Publications
Reviewing status
Peer reviewed