ALT control, delete: FANCM as an anti-cancer target in Alternative Lengthening of Telomeres

Autor:	O’Rourke, Julienne J, Bythell-Douglas, Rohan, Dunn, Elyse A, Deans, Andrew J
Zdroj:	Nucleus; January 2019, Vol. 10 Issue: 1 p221-230, 10p
Abstrakt:	ABSTRACTBreak-induced replication is a specific type of DNA repair that has a co-opted role in telomere extension by telomerase-negative cancer cells. This Alternative Lengthening of Telomeres (or ‘ALT’) is required for viability in approximately 10% of all carcinomas, but up to 50% of the soft-tissue derived sarcomas. In several recent studies, we and others demonstrate that expression and activity of FANCM, a DNA translocase protein, is essential for the viability of ALT-associated cancers. Here we provide a summary of how and why FANCM depletion leads to deletion of ALT-controlled cancers, predominantly through a hyper-activation of break-induced replication. We also discuss how FANCM can and has been targeted in cancer cell killing, including potential opportunities in ALT and other genetic backgrounds.
Databáze:	Supplemental Index
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