Evidence map›Paper›PMID 31122251›Full record

ReviewMolecular cancer2019

The role of necroptosis in cancer biology and therapy.

Yitao Gong, Zhiyao Fan, Guopei Luo, Chao Yang, Qiuyi Huang, Kun Fan, He Cheng, Kaizhou Jin, Quanxing Ni, Xianjun Yu and 1 more

Open access · goldAbstract readReview
In one paragraph

Review in Molecular cancer, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 677 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
677citing papers in PubMed, 6 pooled it
41.5field-weighted citation impact, top 1% of its field
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

677 citing papers in PubMed, 6 syntheses or guidelines pooled it, 1,058 citations in OpenAlex.

  1. Pooled it
  2. Necroptosis in pancreatic cancer: Molecular mechanisms and therapeutic implications.Apoptosis : an international journal on programmed cell death · 2026
    Pooled it
  3. Interaction of HIF-1a with various cell death pathways in tumor immune microenvironment (TIME).Apoptosis : an international journal on programmed cell death · 2026
    Pooled it
  4. Metabolic cell death in cancer: mechanisms and therapeutic potential.Apoptosis : an international journal on programmed cell death · 2025
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617 more citing papers are in PubMed but not listed here.

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 at 3 institutions in 1 country.

Yitao GongDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai, 200032, China.
Zhiyao FanDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai, 200032, China.
Guopei LuoDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai, 200032, China.
Chao YangDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai, 200032, China.
Qiuyi HuangDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai, 200032, China.
Kun FanDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai, 200032, China.
He ChengDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai, 200032, China.
Kaizhou JinDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai, 200032, China.
Quanxing NiDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai, 200032, China.
Xianjun YuDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai, 200032, China. yuxianjun@fudanpci.org.
Chen LiuDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai, 200032, China. liuchen@fudanpci.org.
Shanghai Medical College of Fudan University · CNFudan University Shanghai Cancer Center · CNShanghai Cancer Institute · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Apoptosis resistance is to a large extent a major obstacle leading to chemotherapy failure during cancer treatment. Bypassing the apoptotic pathway to induce cancer cell death is considered to be a promising approach to overcoming this problem. Necroptosis is a regulated necrotic cell death modality in a caspase-independent fashion and is mainly mediated by Receptor-Interacting Protein 1 (RIP1), RIP3, and Mixed Lineage Kinase Domain-Like (MLKL). Necroptosis serves as an alternative mode of programmed cell death overcoming apoptosis resistance and may trigger and amplify antitumor immunity in cancer therapy.The role of necroptosis in cancer is complicated. The expression of key regulators of the necroptotic pathway is generally downregulated in cancer cells, suggesting that cancer cells may also evade necroptosis to survive; however, in certain types of cancer, the expression level of key mediators is elevated. Necroptosis can elicit strong adaptive immune responses that may defend against tumor progression; however, the recruited inflammatory response may also promote tumorigenesis and cancer metastasis, and necroptosis may generate an immunosuppressive tumor microenvironment. Necroptosis also reportedly promotes oncogenesis and cancer metastasis despite evidence demonstrating its antimetastatic role in cancer. In addition, necroptotic microenvironments can direct lineage commitment to determine cancer subtype development in liver cancer. A plethora of compounds and drugs targeting necroptosis exhibit potential antitumor efficacy, but their clinical feasibility must be validated.Better knowledge of the necroptotic pathway mechanism and its physiological and pathological functions is urgently required to solve the remaining mysteries surrounding the role of necroptosis in cancer. In this review, we briefly introduce the molecular mechanism and characteristics of necroptosis, the interplay between necroptosis and other cell death mechanisms, crosstalk of necroptosis and metabolic signaling and detection methods. We also summarize the intricate role of necroptosis in tumor progression, cancer metastasis, prognosis of cancer patients, cancer immunity regulation, cancer subtype determination and cancer therapeutics.

Indexed as

Gene Regulatory NetworksNecroptosisDisease ProgressionGene Expression Regulation, NeoplasticHumansNeoplasmsProtein KinasesReceptor-Interacting Protein Serine-Threonine KinasesTumor MicroenvironmentMLKL protein, humanProtein KinasesReceptor-Interacting Protein Serine-Threonine KinasesRIPK1 protein, humanRIPK3 protein, humanApoptosisAutophagyImmunosuppressionMetastasisMixed lineage kinase domain-like pseudokinase (MLKL)NecroptosisReceptor-interacting protein kinase (RIPK)Therapeutics

Identifiers

PMID31122251
PMCPMC6532150
OpenAlexW2947880033

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.