Evidence map›Paper›PMID 42008190›Full record

SynthesisApoptosis : an international journal on programmed cell death2026

Necroptosis in pancreatic cancer: Molecular mechanisms and therapeutic implications.

Yu-Jie Fan, Wei-Jia Liu, Chang Liu, Yi-Wen Zhu, Ti Chu, Hang-Shen Han, Dong-Dong Wu

Abstract readSystematic Review
PubMed Publisher
In one paragraph

Synthesis in Apoptosis : an international journal on programmed cell death, 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

7 authors.

Yu-Jie Fan *Henan International Joint Laboratory for Nuclear Protein Regulation, School of Stomatology, School of Basic Medical Sciences, Henan University, Kaifeng, 475004, Henan, China.
Wei-Jia Liu *Henan International Joint Laboratory for Nuclear Protein Regulation, School of Stomatology, School of Basic Medical Sciences, Henan University, Kaifeng, 475004, Henan, China.
Chang Liu *Henan International Joint Laboratory for Nuclear Protein Regulation, School of Stomatology, School of Basic Medical Sciences, Henan University, Kaifeng, 475004, Henan, China.
Yi-Wen ZhuHenan International Joint Laboratory for Nuclear Protein Regulation, School of Stomatology, School of Basic Medical Sciences, Henan University, Kaifeng, 475004, Henan, China.
Ti ChuHenan International Joint Laboratory for Nuclear Protein Regulation, School of Stomatology, School of Basic Medical Sciences, Henan University, Kaifeng, 475004, Henan, China.
Hang-Shen HanHenan International Joint Laboratory for Nuclear Protein Regulation, School of Stomatology, School of Basic Medical Sciences, Henan University, Kaifeng, 475004, Henan, China.
Dong-Dong WuHenan International Joint Laboratory for Nuclear Protein Regulation, School of Stomatology, School of Basic Medical Sciences, Henan University, Kaifeng, 475004, Henan, China. ddwubiomed2010@163.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pancreatic ductal adenocarcinoma (PDAC) remains a highly lethal cancer due to its strong resistance to chemotherapeutic agents that induce apoptosis. As conventional treatments gradually lose their effectiveness over time, necroptosis has become a key therapeutic target worth exploiting. Necroptosis is a regulated cell death independent of caspases. It is driven by the receptor-interacting protein kinase 1/3 (RIPK1/3) and mixed lineage kinase domain-like pseudokinase (MLKL) signaling axis. This systematic review summarizes the complex role of necroptosis in PDAC. We clarify how necroptosis can be triggered or manipulated pharmacologically, and how it can be induced by accumulating reactive oxygen species (ROS). We also critically analyze its tumor-promoting side. Persistent necroptotic signaling reshapes the tumor microenvironment (TME) by releasing damage-associated molecular patterns (DAMPs) and activating inflammatory cascades. We also highlight the growing clinical significance of necroptosis-related genes (NRGs), long non-coding RNAs (lncRNAs), and specific biomarkers such as fermitin family member 1 (FERMT1). Finally, we propose a new, context-dependent therapeutic framework. This framework proposes a combination of strategies for controlling necroptosis induction and immunomodulatory agents, offering a reasonable strategy for PDAC management.

Indexed as

Carcinoma, Pancreatic DuctalNecroptosisPancreatic NeoplasmsAnimalsApoptosisHumansProtein KinasesReactive Oxygen SpeciesReceptor-Interacting Protein Serine-Threonine KinasesSignal TransductionTumor MicroenvironmentProtein KinasesReactive Oxygen SpeciesReceptor-Interacting Protein Serine-Threonine KinasesDamage-associated molecular patternsNecroptosisPancreatic ductal adenocarcinomaReactive oxygen speciesTumor microenvironment

Identifiers

PMID42008190

What Socratic 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 Socratic graph.