Evidence map›Paper›PMID 42886347›Full record

ReviewArchives of toxicology2026

Role of PANoptosis in cancer: molecular mechanisms and therapeutic insights.

Yi Zhang, Xue-Li Wang, Yan-Wen Wang, Ti Chu, Lei Cao, Yong-Qi Fan, Yu-Hang Chen, Yan-Ge Li, Wei-Rong Si, Qi-Ying Jiang and 1 more

Abstract readReview
PubMed Publisher
In one paragraph

Review in Archives of toxicology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. 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

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors.

Yi ZhangHenan International Joint Laboratory for Nuclear Protein Regulation, School of Basic Medical Sciences, School of Stomatology, Henan University, Kaifeng, 475004, Henan, China.
Xue-Li WangHenan International Joint Laboratory for Nuclear Protein Regulation, School of Basic Medical Sciences, School of Stomatology, Henan University, Kaifeng, 475004, Henan, China.
Yan-Wen WangHenan International Joint Laboratory for Nuclear Protein Regulation, School of Basic Medical Sciences, School of Stomatology, Henan University, Kaifeng, 475004, Henan, China.
Ti ChuHenan International Joint Laboratory for Nuclear Protein Regulation, School of Basic Medical Sciences, School of Stomatology, Henan University, Kaifeng, 475004, Henan, China.
Lei CaoHenan International Joint Laboratory for Nuclear Protein Regulation, School of Basic Medical Sciences, School of Stomatology, Henan University, Kaifeng, 475004, Henan, China.
Yong-Qi FanHenan International Joint Laboratory for Nuclear Protein Regulation, School of Basic Medical Sciences, School of Stomatology, Henan University, Kaifeng, 475004, Henan, China.
Yu-Hang ChenHenan International Joint Laboratory for Nuclear Protein Regulation, School of Basic Medical Sciences, School of Stomatology, Henan University, Kaifeng, 475004, Henan, China.
Yan-Ge LiHenan International Joint Laboratory for Nuclear Protein Regulation, School of Basic Medical Sciences, School of Stomatology, Henan University, Kaifeng, 475004, Henan, China.
Wei-Rong SiSchool of Basic Medical Sciences, Henan University, Kaifeng, 475004, Henan, China. 10190131@vip.henu.edu.cn.
Qi-Ying JiangHenan International Joint Laboratory for Nuclear Protein Regulation, School of Basic Medical Sciences, School of Stomatology, Henan University, Kaifeng, 475004, Henan, China. jiangqiying365@126.com.
Dong-Dong WuHenan International Joint Laboratory for Nuclear Protein Regulation, School of Basic Medical Sciences, School of Stomatology, Henan University, Kaifeng, 475004, Henan, China. ddwubiomed2010@163.com.

Funding

the National Natural Science Foundation of China 32570850
6 · The paper itself

Abstract

Dysregulated cell death signaling profoundly influences oncogenesis, making the targeted elimination of malignant cells a cornerstone of modern oncological interventions. Insights into programmed cell death kinetics have revealed cross-talk among apoptosis, pyroptosis, and necroptosis, establishing the conceptual framework of PANoptosis. As an inflammatory death modality, PANoptosis is orchestrated by a multi-subunit protein platform termed the PANoptosome, which integrates and executes these distinct death programs. This review outlines the fundamental molecular cascades governing PANoptosis, alongside its multifaceted involvement in tumorigenesis, immune microenvironment remodeling, and metastatic dissemination. Although PANoptosis potentiates host antitumor defense mechanisms, its impact on malignant progression remains context-dependent. Pharmacological intervention directed at central node molecules or combined with radiation and immune checkpoint blockade represents a compelling strategy. Notably, suppressing ZBP1 attenuates chemotherapy-induced systemic toxicities, whereas multimodal therapies synergistically augment therapeutic efficacy. Nevertheless, precise regulatory networks demand further elucidation, and clinical translation requires rigorous validation. Ultimately, PANoptosis offers novel insights into cancer biology and paves the way for personalized therapeutic paradigms.

Indexed as

CancerCombination therapyPANoptosisTargeted therapy

Identifiers

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.