Evidence map›Paper›PMID 27048810›Full record

ReviewCellular and molecular life sciences : CMLS2016

Cancer and necroptosis: friend or foe?

Stephan Philipp, Justyna Sosna, Dieter Adam

Abstract readReview
In one paragraph

Review in Cellular and molecular life sciences : CMLS, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed, 1 pooled it
–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

52 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Metabolic cell death in cancer: mechanisms and therapeutic potential.Apoptosis : an international journal on programmed cell death · 2025
    Pooled it
  2. Review
  3. MMP14-Dependent Activation of TGF-β Signaling Enhances Malignancies via Promoting Necroptosis in Glioblastoma.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Renalase alleviates salt-induced kidney necroptosis and inflammation.Hypertension research : official journal of the Japanese Society of Hypertension · 2024
    Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. The double-edged functions of necroptosis.Cell death & disease · 2023
    Review
  14. Review
  15. Article
  16. Necroptosis: A Pathogenic Negotiator in Human Diseases.International journal of molecular sciences · 2022
    Review
  17. Blood index panel for gastric cancer detection.World journal of gastrointestinal surgery · 2022
    Article
  18. Article
  19. Article
  20. Article
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

3 authors.

Stephan PhilippInstitut für Immunologie, Christian-Albrechts-Universität, Michaelisstraße 5, 24105, Kiel, Germany.
Justyna SosnaInstitut für Immunologie, Christian-Albrechts-Universität, Michaelisstraße 5, 24105, Kiel, Germany.
Dieter AdamInstitut für Immunologie, Christian-Albrechts-Universität, Michaelisstraße 5, 24105, Kiel, Germany. dadam@email.uni-kiel.de.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Regulated cell death is one major factor to ensure homoeostasis in multicellular organisms. For decades, apoptosis was considered as the sole form of regulated cell death, whereas necrosis was believed to be accidental and unregulated. Due to this view, research on necrosis was somewhat neglected, especially in the field of anti-cancer treatment. However, new interest in necrosis has been sparked by the recent discovery of different forms of necrosis that show indeed regulated pathways. More and more studies now address the molecular pathways of regulated necrosis and its connections within the cellular signaling networks. Necroptosis, a subform of regulated necrosis, has so far hardly been focused on with regard to a future treatment of cancer patients and may emerge as a novel and effective approach to eliminate tumor cells. However, and similar to apoptosis, tumor cells can develop resistances against necroptosis to ensure their own survival. In this context, new molecules that enhance necroptosis are currently being identified to overcome such resistances. This review discusses cancer and necroptosis as friends or foes, i.e. the options to exploit necroptosis in anti-cancer therapies ("foes"), but also potential limitations that may block or actually cause necroptosis to act in a protumoral manner ("friends"). The balance between these two possible roles will determine whether necroptosis can indeed be used as a promising tool for early diagnosis of tumors, prevention of metastasis and anti-cancer treatment.

Indexed as

ApoptosisHumansNecrosisNeoplasmsSignal TransductionTNF-Related Apoptosis-Inducing LigandTumor Necrosis Factor-alphaTNF-Related Apoptosis-Inducing LigandTNFSF10 protein, humanTumor Necrosis Factor-alphaCancerNecroptosisRegulated necrosisTNFTRAIL

Identifiers

PMID27048810
PMCPMC11108265

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.