Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.6.1.2 (alanine aminotransferase)
26,722 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We recently reported that depletion of FANCM in ALT cells induces replication stress mainly at their telomeres. Additionally, we found that co-depletion of FANCM and BLM, or FANCM and BRCA1 induces synthetic lethality in the ALT cells. Our new findings could have important implications for cancer prevention and treatment.
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PMID:Breaking the end: Target the replication stress response at the ALT telomeres for cancer therapy. 2920 49

Break-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.
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PMID:ALT control, delete: FANCM as an anti-cancer target in Alternative Lengthening of Telomeres. 3238 67