Journal
TRENDS IN CANCER
Volume 1, Issue 3, Pages 161-173Publisher
CELL PRESS
DOI: 10.1016/j.trecan.2015.10.002
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Funding
- National Institutes of Health/National Cancer Institute (NIH/NCI) [7P01CA095616-10, CPRITRP140612, NIH CDP SPORE P50CA127001-07]
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Genomic deletion of tumor suppressor genes (TSGs) is a rite of passage for virtually all human cancers. The synthetic lethal paradigm has provided a framework for the development of molecular targeted therapeutics that are functionally linked to the loss of specific TSG functions. In the course of genomic events that delete TSGs, a large number of genes with no apparent direct role in tumor promotion also sustain deletion as a result of chromosomal proximity to the target TSG. In this perspective, we review the novel concept of 'collateral lethality', which has served to identify cancer-specific therapeutic vulnerabilities resulting from codeletion of passenger genes neighboring TSGs. The large number of collaterally deleted genes, playing diverse functions in cell homeostasis, offers a rich repertoire of pharmacologically targetable vulnerabilities presenting novel opportunities for the development of personalized antineoplastic therapies.
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