ArticleScience advances2026
Sensitizing tumor response to topoisomerase I antibody-drug conjugate by selective CDK7 inhibition.
Article in Science advances, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
This study investigates the transcriptional impact of Q901, a highly selective cyclin-dependent kinase 7 (CDK7) inhibitor in clinical development. Q901 primarily disrupted MYC and E2F-dependent transcription programs, down-regulating cell cycle control and DNA damage repair pathways. CDK7 binding at the promoter-proximal regions was markedly stabilized by Q901, leading to reduced occupancy of MYC, E2F, and RNA polymerase II (RNAPII). These findings offered a novel therapeutic strategy to enhance cancer susceptibility to topoisomerase I (TOP1) DNA-protein cross-links (TOP1-DPCs) induced by TOP1 inhibitors. Resistance to TOP1 inhibitors arises through activation of DNA repair pathways when elongating RNAPII encounters TOP1-DPCs. By suppressing RNAPII transition from initiation to elongation and DNA repair pathways, Q901 stabilizes TOP1-DPCs and sensitizes tumors to TOP1 inhibitors. Preclinical studies demonstrated enhanced tumor suppression when combining Q901 with TOP1 inhibitor-based antibody-drug conjugates (TOP1i-ADCs), highlighting its potential as a therapeutic option for cancers resistant to TOP1i-ADC therapy.
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