Cancer cell plasticity due to the dynamic architecture of protein-protein interactions networks (i.e. interactomes) provides a vexing outlet for therapy evasion. Joshi et al show how forcing interactomes into a state where no rebound pathways can be deployed renders therapeutics with traditionally poor performance to become highly efficacious.
Chromosomal instability (CIN) is a hallmark of cancer and has been associated with a highly metastatic phenotype in numerous cancers. We identified a novel function for APOBEC3A in the initiation of CIN featuring enhanced, STING-dependent, distant organ seeding, and metastatic growth.
Our recent study revealed that the chemotherapeutic CX-5461 primarily binds and inhibits TOP2B, exhibiting selective cytotoxicity in neuroblastoma cells, which overexpress TOP2B. As such, pharmacological targeting of TOP2B raises safety concerns due to off-target drug interactions with this gene.
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