Evidence map›Paper›PMID 18442364›Full record

ArticleMolecular cancer2008

Transcription analysis in the MeLiM swine model identifies RACK1 as a potential marker of malignancy for human melanocytic proliferation.

Giorgia Egidy, Sophia Julé, Philippe Bossé, Florence Bernex, Claudine Geffrotin, Silvia Vincent-Naulleau, Vratislav Horak, Xavier Sastre-Garau, Jean-Jacques Panthier

Open access · goldAbstract read
In one paragraph

Article in Molecular cancer, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

24 citing papers in PubMed, 44 citations in OpenAlex.

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  8. The Apoptotic, Angiogenic and Cell Proliferation Genes CD63, S100A6 e GNB2L1 are Altered in Patients with Endometriosis.Revista brasileira de ginecologia e obstetricia : revista da Federacao Brasileira das Sociedades de Ginecologia e Obstetricia · 2018
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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

9 authors at 7 institutions in 2 countries.

Giorgia EgidyINRA, UMR955 Génétique Moléculaire et Cellulaire; Laboratoire conventionné CEA n degree 17; Ecole Nationale Vétérinaire d'Alfort, 7 avenue du Général de Gaulle, Maisons-Alfort, F-94704 France. gegidy@pasteur.fr
Sophia Julé
Philippe Bossé
Florence Bernex
Claudine Geffrotin
Silvia Vincent-Naulleau
Vratislav Horak
Xavier Sastre-Garau
Jean-Jacques Panthier
Commissariat à l'Énergie Atomique et aux Énergies Alternatives · FRMathématiques et Informatique Appliquées du Génome à l'Environnement · FRCzech Academy of Sciences, Institute of Animal Physiology and Genetics · CZÉcole Nationale Vétérinaire d'Alfort · FRInstitut Curie · FRLaboratoire de Biologie du Développement · FRLaboratoire de Génétique Cellulaire · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMetastatic melanoma is a severe disease. Few experimental animal models of metastatic melanoma exist. MeLiM minipigs exhibit spontaneous melanoma. Cutaneous and metastatic lesions are histologically similar to human's. However, most of them eventually spontaneously regress. Our purpose was to investigate whether the MeLiM model could reveal markers of malignancy in human melanocytic proliferations.

resultsWe compared the serial analysis of gene expression (SAGE) between normal pig skin melanocytes and melanoma cells from an early pulmonary metastasis of MeLiM minipigs. Tag identification revealed 55 regulated genes, including GNB2L1 which was found upregulated in the melanoma library. In situ hybridisation confirmed GNB2L1 overexpression in MeLiM melanocytic lesions. GNB2L1 encodes the adaptor protein RACK1, recently shown to influence melanoma cell lines tumorigenicity. We studied the expression of RACK1 by immunofluorescence and confocal microscopy in tissues specimens of normal skin, in cutaneous and metastatic melanoma developped in MeLiM minipigs and in human patients. In pig and human samples, the results were similar. RACK1 protein was not detected in normal epidermal melanocytes. By contrast, RACK1 signal was highly increased in the cytoplasm of all melanocytic cells of superficial spreading melanoma, recurrent dermal lesions and metastatic melanoma. RACK1 partially colocalised with activated PKCalphabeta. In pig metastases, additional nuclear RACK1 did not associate to BDNF expression. In human nevi, the RACK1 signal was low.

conclusionRACK1 overexpression detected in situ in human melanoma specimens characterized cutaneous and metastatic melanoma raising the possibility that RACK1 can be a potential marker of malignancy in human melanoma. The MeLiM strain provides a relevant model for exploring mechanisms of melanocytic malignant transformation in humans. This study may contribute to a better understanding of melanoma pathophysiology and to progress in diagnosis.

Indexed as

Cell ProliferationTranscription, GeneticAnimalsBiomarkers, TumorDisease Models, AnimalEnzyme ActivationFemaleGTP-Binding ProteinsHumansIn Situ HybridizationMaleMelanocytesMelanomaMicroscopy, ConfocalNeoplasm ProteinsProtein Kinase CBiomarkers, TumorGTP-Binding ProteinsNeoplasm ProteinsProtein Kinase CRACK1 protein, humanReceptors, Cell SurfaceReceptors for Activated C KinaseRNA, Messenger

Identifiers

PMID18442364
PMCPMC2387171
OpenAlexW2161965202

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.