Transcriptional remodeling shapes therapeutic vulnerability to necroptosis in acute lymphoblastic leukemia.

ABSTRACT:

Abstract

Insufficient eradication of cancer cells and survival of drug tolerant clones are major relapse driving forces. Underlying molecular mechanisms comprise activated prosurvival and antiapoptotic signaling, leading to insufficient apoptosis and drug resistance. The identification of programmed cell death pathways alternative to apoptosis opens up possibilities to antagonize apoptosis escape routes. We have earlier shown that acute lymphoblastic leukemia (ALL) harbors a distinct propensity to undergo cell death by receptor-interacting protein kinase 1 (RIPK1)-dependent necroptosis, activated by small-molecule second mitochondria-derived activators of caspase (SMAC) mimetics. Despite demonstrated safety and tolerability of SMAC mimetics in clinical trials, their efficacy as sin

SUBMITTER: Saorin A 

PROVIDER: S-EPMC12783532 | biostudies-literature | 2025 Aug

REPOSITORIES: biostudies-literature