Evidence map›Paper›PMID 41610314›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026

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

Xiaoling Xu, WeiYi Cheng, Menghang Yang, Li He, WeiYe Ren, JingQuan Chen, LiTing He, Dandan Bao, Zhihong Zhu, Lixin Wang and 2 more

Erratum issuedAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors.

Xiaoling XuDepartment of Radiation Oncology, Shanghai Pulmonary Hospital, Tongji University School of Medicine, Shanghai, China.
WeiYi ChengSchool of Pharmaceutical Sciences, The First Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, Zhejiang, China.
Menghang YangDepartment of Radiation Oncology, Shanghai Pulmonary Hospital, Tongji University School of Medicine, Shanghai, China.
Li HeSchool of Pharmaceutical Sciences, The First Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, Zhejiang, China.
WeiYe RenSchool of Pharmaceutical Sciences, The First Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, Zhejiang, China.
JingQuan ChenSchool of Pharmaceutical Sciences, The First Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, Zhejiang, China.
LiTing HeSchool of Pharmaceutical Sciences, The First Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, Zhejiang, China.
Dandan BaoSchool of Pharmaceutical Sciences, The First Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, Zhejiang, China.
Zhihong ZhuSchool of Pharmaceutical Sciences, The First Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, Zhejiang, China.
Lixin WangDepartment of Integrative Medicine, Shanghai Pulmonary Hospital, Tongji University School of Medicine, Shanghai, China.
Qinghua YaoDepartment of Oncology, The Second Affiliated Hospital of Zhejiang Chinese Medical University, Xinhua Hospital of Zhejiang Province, Hangzhou, Zhejiang, China.
Ji-Gang PiaoSchool of Pharmaceutical Sciences, The First Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, Zhejiang, China.ORCID https://orcid.org/0000-0002-4280-0634

Funding

National Administration of Traditional Chinese Medicine Project for the Construction of Flagship Departments for Integrative Medicine 2024National Natural Science Foundation of China 82104405Natural Science Foundation of Hangzhou 2024SZRYBH160002Natural Science Foundation of Shanghai 25ZR1402449Natural Science Foundation of Zhejiang Province LY23H300002Shanghai Key Discipline of Traditional Chinese Medicine shzyyzdxk-2024106
6 · The paper itself

Abstract

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, allicin, a natural ATR inhibitor and hydrogen sulfide (H

Indexed as

DisulfidesLiposomesLung NeoplasmsSulfinic AcidsTumor Suppressor Protein p53AnimalsAntineoplastic AgentsCell Line, TumorHumansMiceMutationallicinAntineoplastic AgentsDisulfidesLiposomesSulfinic AcidsTumor Suppressor Protein p53allicinDNA damage response (DDR)Lung cancerp53 mutationSynthetic lethality

Identifiers

PMID41610314
PMCPMC13042845

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.