Evidence map›Paper›PMID 10523621›Full record

ArticleMolecular and cellular biology1999

DNA methylation is the primary silencing mechanism for a set of germ line- and tumor-specific genes with a CpG-rich promoter.

C De Smet, C Lurquin, B Lethé, V Martelange, T Boon

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 228 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
228citing papers in PubMed, 2 pooled it
7.1field-weighted citation impact, top 2% 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

228 citing papers in PubMed, 2 syntheses or guidelines pooled it, 592 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Trial
  5. Review
  6. Cross-Species Upregulation ofCurrent issues in molecular biology · 2026
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  7. Review
  8. Article
  9. DNA-demethylation by DAC inducesMolecular therapy. Oncology · 2025
    Article
  10. Hsp90Pharmaceuticals (Basel, Switzerland) · 2025
    Review
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Review
  18. Article
  19. Review
  20. Review

168 more citing papers are in PubMed but not listed here.

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

5 authors at 1 institution in 1 country.

C De SmetLudwig Institute for Cancer Research, Brussels Branch, Brussels B-1200, Belgium.
C Lurquin
B Lethé
V Martelange
T Boon
Ludwig Cancer Research · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A subset of male germ line-specific genes, the MAGE-type genes, are activated in many human tumors, where they produce tumor-specific antigens recognized by cytolytic T lymphocytes. Previous studies on gene MAGE-A1 indicated that transcription factors regulating its expression are present in all tumor cell lines whether or not they express the gene. The analysis of two CpG sites located in the promoter showed a strong correlation between expression and demethylation. It was also shown that MAGE-A1 transcription was induced in cell cultures treated with demethylating agent 5'-aza-2'-deoxycytidine. We have now analyzed all of the CpG sites within the 5' region of MAGE-A1 and show that for all of them, demethylation correlates with the transcription of the gene. We also show that the induction of MAGE-A1 with 5'-aza-2'-deoxycytidine is stable and that in all the cell clones it correlates with demethylation, indicating that demethylation is necessary and sufficient to produce expression. Conversely, transfection experiments with in vitro-methylated MAGE-A1 sequences indicated that heavy methylation suffices to stably repress the gene in cells containing the transcription factors required for expression. Most MAGE-type genes were found to have promoters with a high CpG content. Remarkably, although CpG-rich promoters are classically unmethylated in all normal tissues, those of MAGE-A1 and LAGE-1 were highly methylated in somatic tissues. In contrast, they were largely unmethylated in male germ cells. We conclude that MAGE-type genes belong to a unique subset of germ line-specific genes that use DNA methylation as a primary silencing mechanism.

Indexed as

CpG IslandsDNA MethylationGene Expression Regulation, NeoplasticGene SilencingPromoter Regions, GeneticAzacitidineDecitabineDNA, NeoplasmHumansMaleNeoplasm ProteinsSpermatozoaTestisTissue DistributionTumor Cells, CulturedAzacitidineDecitabineDNA, NeoplasmNeoplasm Proteins

Identifiers

PMID10523621
PMCPMC84726
OpenAlexW2116646376

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.