Evidence map›Paper›PMID 42542455›Full record

ArticleCell death & disease2026

The anti-tumour activity of TNF in melanoma is determined by cFLIP.

Johanna Stachelscheid, Cäcilia Kaul, Katrin Gerstenberg, J Paul Werthenbach, Fabian Schorn, Joy Steinkamp, Paola Zigrino, Manolis Pasparakis, Lars M Schiffmann, Hamid Kashkar

Abstract read
In one paragraph

Article in Cell death & disease, 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

10 authors.

Johanna Stachelscheid *University of Cologne, Faculty of Medicine and University Hospital of Cologne, Institute for Molecular Immunology, Cologne, Germany.ORCID http://orcid.org/0000-0001-7419-8900
Cäcilia Kaul *University of Cologne, Faculty of Medicine and University Hospital of Cologne, Institute for Molecular Immunology, Cologne, Germany.ORCID http://orcid.org/0000-0001-8239-5576
Katrin GerstenbergUniversity of Cologne, Faculty of Medicine and University Hospital of Cologne, Institute for Molecular Immunology, Cologne, Germany.
J Paul WerthenbachUniversity of Cologne, Faculty of Medicine and University Hospital of Cologne, Institute for Molecular Immunology, Cologne, Germany.
Fabian SchornUniversity of Cologne, Faculty of Medicine and University Hospital of Cologne, Institute for Molecular Immunology, Cologne, Germany.
Joy SteinkampDepartment of Dermatology and Venereology, University of Cologne, Faculty of Medicine and University Hospital of Cologne, Cologne, Germany.ORCID http://orcid.org/0000-0001-9842-3818
Paola ZigrinoDepartment of Dermatology and Venereology, University of Cologne, Faculty of Medicine and University Hospital of Cologne, Cologne, Germany.
Manolis PasparakisUniversity of Cologne, Faculty of Mathematics and Natural Sciences, Institute for Genetics, Cologne, Germany.ORCID http://orcid.org/0000-0002-9870-0966
Lars M SchiffmannUniversity of Cologne, Faculty of Medicine and University Hospital of Cologne, Department of General, Visceral, Thoracic and Transplant Surgery, Cologne, Germany.
Hamid KashkarUniversity of Cologne, Faculty of Medicine and University Hospital of Cologne, Institute for Molecular Immunology, Cologne, Germany. h.kashkar@uni-koeln.de.ORCID http://orcid.org/0000-0003-2796-1429

Funding

Deutsche Forschungsgemeinschaft (German Research Foundation) 269925409Deutsche Forschungsgemeinschaft (German Research Foundation) 414786233Deutsche Forschungsgemeinschaft (German Research Foundation) 455784452Deutsche Forschungsgemeinschaft (German Research Foundation) 501530074Deutsche Krebshilfe (German Cancer Aid) 70114225Deutsche Krebshilfe (German Cancer Aid) 70117362Deutsche Krebshilfe (German Cancer Aid) 70117363
6 · The paper itself

Abstract

Tumour necrosis factor (TNF) is a pleiotropic cytokine originally identified for its ability to kill cancer cells. However, a paradoxical tumour-promoting role for TNF emerged when early attempts to exploit its anti-tumour activity in cancer therapy produced conflicting outcomes, raising the question of whether TNF should be viewed as a therapeutic agent or a treatment target in cancer. Here, we demonstrate that expression of cFLIP, a catalytically inactive paralogue of caspase-8 (CASP8), determines the susceptibility of melanoma cells to TNF and thereby controls melanoma growth in a syngeneic, immune-competent mouse model of B16F10 cutaneous melanoma. B16F10 melanoma cells lacking cFLIP (cFlip

Indexed as

CASP8 and FADD-Like Apoptosis Regulating ProteinMelanomaMelanoma, ExperimentalTumor Necrosis Factor-alphaAnimalsApoptosisCell Line, TumorHumansMiceMice, Inbred C57BLMice, KnockoutCASP8 and FADD-Like Apoptosis Regulating ProteinTumor Necrosis Factor-alpha

Identifiers

PMID42542455
PMCPMC13428747

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.