Evidence map›Paper›PMID 12101411›Full record

ArticleOncogene2002

Tumour necrosis factor-alpha mediates tumour promotion via a PKC alpha- and AP-1-dependent pathway.

Caroline H Arnott, Kate A Scott, Robert J Moore, Alan Hewer, David H Phillips, Peter Parker, Frances R Balkwill, David M Owens

Abstract readComparative Study
PubMed Publisher
In one paragraph

Article in Oncogene, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

50 citing papers in PubMed, 165 citations in OpenAlex.

  1. Review
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  16. Journal of oral microbiology · 2019
    Article
  17. Article
  18. Chronic Inflammation in Skin Malignancies.Journal of molecular signaling · 2016
    Review
  19. Article
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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

8 authors at 4 institutions in 1 country.

Caroline H ArnottCancer Research UK Translational Oncology Laboratory, Bart's and The London School of Medicine and Dentistry, Queen Mary, University of London, John Vane Science Centre, Charterhouse Square, London EC1M 6BQ, UK.
Kate A Scott
Robert J Moore
Alan Hewer
David H Phillips
Peter Parker
Frances R Balkwill
David M Owens
Cancer Research UK · GBInstitute of Cancer Research · GBQueen Mary University of London · GBThe Honourable Society of Lincoln's Inn · GB

Funding

SUPRABASAL INTEGRIN EXPRESSION IN EPIDERMAL NEOPLASIAF32CA075638 · NCI · IMPERIAL CANCER RESEARCH FUND · PI OWENS, DAVID M · 1998 to 2000
$39k
NCI NIH HHS CA75638
6 · The paper itself

Abstract

Tumour necrosis factor-alpha (TNF-alpha) deficient mice (TNF-alpha(-/-) mice) are resistant to skin carcinogenesis. Cellular signalling via the transcription factor complex AP-1 is thought to play a key role in tumour promotion. The induction of a specific subset of AP-1 responsive genes thought to be important for tumour development, namely GM-CSF, MMP-9 and MMP-3, was suppressed in TNF-alpha(-/-) compared to wild-type mouse skin in response to the tumour promotor TPA. The differential induction of these genes correlated with a temporal shift in AP-1 activation and c-Jun expression in TNF-alpha(-/-) compared to wild-type epidermis. The major receptor for TPA-induced signalling in basal keratinocytes, PKC alpha, was also differentially regulated in wild-type compared with TNF-alpha(-/-) epidermis. A marked delay in TPA-induced intracellular translocation and downregulation of PKC alpha was observed in TNF-alpha(-/-) epidermis, which correlated with the deregulated TPA-induced AP-1 activation and c-Jun expression. The frequency of DNA adduct formation and c-Ha-ras mutations was the same in wild-type and TNF-alpha(-/-) epidermis after DMBA treatment, suggesting that TNF-alpha was not involved in tumour initiation. These data suggest that the pro-inflammatory cytokine TNF-alpha is a critical mediator of tumour promotion, acting via a PKC alpha- and AP-1-dependent pathway. This may be one mechanism by which chronic inflammation increases susceptibility to cancer.

Indexed as

Carcinogens9,10-Dimethyl-1,2-benzanthraceneAnimalsEpidermal CellsEpidermisIsoenzymesKeratinocytesKineticsMatrix MetalloproteinasesMiceMice, Inbred BALB CMice, KnockoutProtein Kinase CProtein Kinase C-alphaRNA, MessengerSignal Transduction9,10-Dimethyl-1,2-benzanthraceneCarcinogensIsoenzymesMatrix MetalloproteinasesPrkca protein, mouseProtein Kinase CProtein Kinase C-alphaRNA, MessengerTetradecanoylphorbol AcetateTranscription Factor AP-1Tumor Necrosis Factor-alpha

Identifiers

PMID12101411
OpenAlexW207000493

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.