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Pro-ATO/Allicin Liposomes for Dual-Pathway Targeting of p53-Mutant Tumors.

Advanced science (Weinheim, Baden-Wurttemberg, Germany) - 1 Mar 2026

Xu Xiaoling, Cheng WeiYi, Yang Menghang, He Li, Ren WeiYe, Chen JingQuan, He LiTing, Bao Dandan, Zhu Zhihong, Wang Lixin, Yao Qinghua, Piao Ji-Gang

Abstract excerpt

Mutations in the tumor suppressor p53 disrupt DNA damage response (DDR) and drive therapeutic resistance in lung cancer. Although arsenic trioxide (ATO) can restore transcriptional activity of structural p53 mutants, its clinical application is limited by subtype selectivity and systemic toxicity. In parallel, p53 deficiency creates dependence on S/G2 checkpoints, rendering ATR a synthetic lethal target; however,...

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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Identifiers

PMID: 41610314
DOI: 10.1002/advs.202519194
PMCID: PMC13042845

Genes

ATR

Variants

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026.

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