Evidence map›Paper›PMID 18592010›Full record

ArticleNeoplasia (New York, N.Y.)2008

Gene expression signature for spontaneous cancer regression in melanoma pigs.

Florian Rambow, Guillaume Piton, Stephan Bouet, Jean-Jaques Leplat, Sylvain Baulande, Angelique Marrau, Mark Stam, Vratislav Horak, Silvia Vincent-Naulleau

Open access · goldAbstract readComparative StudyValidation Study
In one paragraph

Article in Neoplasia (New York, N.Y.), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
3.3field-weighted citation impact, top 10% 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

20 citing papers in PubMed, 33 citations in OpenAlex.

  1. Review
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  5. Transcription from a gene desert in a melanoma porcine model.Molecular genetics and genomics : MGG · 2020
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  7. Review
  8. Review
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  11. Review
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  14. Genetic and functional evaluation of MITF as a candidate gene for cutaneous melanoma predisposition in pigs.Mammalian genome : official journal of the International Mammalian Genome Society · 2011
    Article
  15. Article
  16. The War on Cancer rages on.Neoplasia (New York, N.Y.) · 2009
    Article
  17. Article
  18. Neoplasia: the second decade.Neoplasia (New York, N.Y.) · 2008
    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

9 authors at 4 institutions in 2 countries.

Florian RambowINRA, UMR 314, Laboratoire de Radiobiologie et d'Etude du Génome, F-78350 Jouy-en-Josas, France. florian.rambow@jouy.inra.fr
Guillaume Piton
Stephan Bouet
Jean-Jaques Leplat
Sylvain Baulande
Angelique Marrau
Mark Stam
Vratislav Horak
Silvia Vincent-Naulleau
Commissariat à l'Énergie Atomique et aux Énergies Alternatives · FRInstitut de Radiobiologie Cellulaire et Moléculaire · FRGenopole (France) · FRCzech Academy of Sciences, Institute of Animal Physiology and Genetics · CZ

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Incomplete spontaneous regression of melanoma is common. However, complete melanoma regression is still a very rare phenomenon. Because melanoma is the most immunogenic human malignancy, the mechanisms leading to regression, based on accumulative evidence, are the host's immune responses. Unfortunately, therapies aiming to enhance the patient's natural immunity against melanoma have yet to meet their expectations. Reasons for failure include various immune escape mechanisms, induced by the tumor, that subsequently lead to tolerance. Here, we performed time-dependent gene expression profiling to unravel molecular changes involved in the transition of progressive melanoma to complete tumor regression using a porcine model. The melanoblastomabearing Libechov minipigs are highly suitable for this study because these animals exhibit naturally occurring and regressing melanomas. We were able to identify a molecular signature of the melanoma regression process. Genes regulated in this signature were associated with 1) cell cycle, 2) immune response, and 3) melanocyte differentiation. These genes may shed light on molecular mechanisms involved in complete melanoma regression and indicate what improvements are needed for successful antimelanoma therapy.

Indexed as

Gene Expression ProfilingAnimalsCluster AnalysisGene Expression Regulation, NeoplasticGenes, MHC Class IIHumansMelanomaNeoplasm Regression, SpontaneousOligonucleotide Array Sequence AnalysisSwineTime Factors

Identifiers

PMID18592010
PMCPMC2435007
OpenAlexW1231578283

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.