Synthetic Lethality-based Targets for Discovery of New Cancer Therapeutics

Cancer Genomics - Proteomics

Ulrich H. Weidle²  Daniela Maisel²  Dirk Eick¹ 

[1] Department of Epigenetics, Center for Integrated Protein Science Munich (CIPSM), Helmholtz Center Munich, Munich, GermanyDepartment of Epigenetics, Center for Integrated Protein Science Munich (CIPSM), Helmholtz Center Munich, Munich, GermanyDepartment of Epigenetics, Center for Integrated Protein Science Munich (CIPSM), Helmholtz Center Munich, Munich, Germany;Roche Diagnostics, Division Pharma, Penzberg, GermanyRoche Diagnostics, Division Pharma, Penzberg, GermanyRoche Diagnostics, Division Pharma, Penzberg, Germany

关键词: DNA repair;    oncogenes;    poly(ADP) ribose polymerase;    protein kinase networks;    tumor suppressor genes;    review;   

DOI  :  

来源: Delinasios GJ CO

【 摘 要 】

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.

【 授权许可】

Unknown