ArticleFrontiers in pharmacology2026
Paclitaxel-induced germline DNA-damage signatures independent of mismatch repair in
Article in Frontiers in pharmacology, 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
Introduction: Paclitaxel is a frontline chemotherapeutic agent that stabilizes microtubules, but its broader impact on germline genome stability and long-term tolerance mechanisms remains incompletely understood. Methods: Using Results: Paclitaxel markedly impaired fertility: hatching dropped approximately 54%, larval arrest increased approximately 4.1-fold, and brood size decreased approximately 31% at 50 μM (all P < 0.01). HIM progeny rose 15-fold, with 52% of nuclei lacking SYP-1 and widespread abnormal chromosome clustering. RAD-51 foci persisted and late-pachytene apoptosis increased 47%, indicating defective DNA damage repair. Transcriptomic analysis revealed upregulation of detoxification and immune pathways and selective downregulation of mismatch repair genes; however, genetic manipulation confirmed that MMR attenuation is a stress signature rather than a causal driver. Multigenerational exposure led to initial sensitization (F5 survival 18.9%) followed by partial recovery (F10 survival 60.1%). Parallel experiments in human kidney cancer cells revealed concentration-dependent apoptosis, reflecting the phenotypes observed in nematodes. Conclusion: This integrated analysis establishes
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