Evidence map›Paper›PMID 12545168›Full record

ArticleOncogene2003

Frequent epigenetic inactivation of the RASSF1A tumour suppressor gene in testicular tumours and distinct methylation profiles of seminoma and nonseminoma testicular germ cell tumours.

Sofia Honorio, Angelo Agathanggelou, Nicolas Wernert, Marcus Rothe, Eamonn R Maher, Farida Latif

Abstract read
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In one paragraph

Article in Oncogene, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 2 pooled it
4.4field-weighted citation impact, top 5% 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

34 citing papers in PubMed, 2 syntheses or guidelines pooled it, 117 citations in OpenAlex.

  1. Pooled it
  2. Association BetweenCancer genomics & proteomics
    Pooled it
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Epigenetically inactivated RASSF1A as a tumor biomarker.Bosnian journal of basic medical sciences · 2021
    Review
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  10. Review
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Molecular genetics of testicular germ cell tumors.American journal of cancer research · 2012
    Article
  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

6 authors at 3 institutions in 2 countries.

Sofia HonorioSection of Medical and Molecular Genetics, Department of Paediatrics and Child Health, University of Birmingham, The Medical School, Edgbaston, UK.
Angelo Agathanggelou
Nicolas Wernert
Marcus Rothe
Eamonn R Maher
Farida Latif
University of Birmingham · GBUniversity of Bonn · DECancer Research UK · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Testicular germ cell tumours (TGCTs) are histologically heterogeneous neoplasms with variable malignant potential. Previously, we demonstrated frequent 3p allele loss in TGCTs, and recently we and others have shown that the 3p21.3 RASSF1A tumour suppressor gene (TSG) is frequently inactivated by promoter hypermethylation in a wide range of cancers including lung, breast, kidney and neuroblastoma. In order to investigate the role of epigenetic events in the pathogenesis of TGCTs, we analysed the promoter methylation status of RASSF1A and nine other genes that may be epigenetically inactivated in cancer (p16(INK4A), APC, MGMT, GSTP1, DAPK, CDH1, CDH13, RARbeta and FHIT) in 24 primary TGCTs (28 histologically distinct components). RASSF1A methylation was detected in four of 10 (40%) seminomas and 15 of 18 (83%) nonseminoma TGCT (NSTGCT) components (P=0.0346). None of the other nine candidate genes were methylated in seminomas, but MGMT (44%), APC (29%) and FHIT (29%) were frequently methylated in NSTGCTs. Furthermore, in two mixed germ cell tumours, the NSTGCT component for one demonstrated RASSF1A, APC and CDH13 promoter methylation, but the seminoma component was unmethylated for all genes analysed. In the second mixed germ cell tumour, the NSTGCT component was methylated for RASSF1A and MGMT, while the seminoma component was methylated only for RASSF1A. In all, 61% NSTGCT components but no seminoma samples demonstrated promoter methylation at two or more genes (P=0.0016). These findings are consistent with a multistep model for TGCT pathogenesis in which RASSF1A methylation occurs early in tumorigenesis and additional epigenetic events characterize progression from seminoma to NSTGCTs.

Indexed as

Acid Anhydride HydrolasesDNA MethylationTumor Suppressor ProteinsAdenomatous Polyposis Coli ProteinBis(5'-adenosyl)triphosphataseCadherinsGene Expression Regulation, NeoplasticGene SilencingGenes, Tumor SuppressorHumansMaleNeoplasm ProteinsNeoplasms, Germ Cell and EmbryonalO(6)-Methylguanine-DNA MethyltransferasePromoter Regions, GeneticSeminomaAcid Anhydride HydrolasesAdenomatous Polyposis Coli ProteinBis(5'-adenosyl)triphosphataseCadherinsH-cadherinNeoplasm ProteinsO(6)-Methylguanine-DNA MethyltransferaseRASSF1 protein, humanTumor Suppressor Proteins

Identifiers

PMID12545168
OpenAlexW2093497966

What OpenQuestion holds

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Read underepoch 390

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.