Evidence map›Paper›PMID 20072159›Full record

ArticleLeukemia2010

Epigenetic plasticity of hTERT gene promoter determines retinoid capacity to repress telomerase in maturation-resistant acute promyelocytic leukemia cells.

A Azouz, Y-L Wu, J Hillion, I Tarkanyi, A Karniguian, J Aradi, M Lanotte, G-Q Chen, M Chehna, E Ségal-Bendirdjian

Abstract read
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In one paragraph

Article in Leukemia, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

19 citing papers in PubMed, 30 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Biomedicines · 2022
    Article
  6. Article
  7. Article
  8. Diverse regulatory manners of human telomerase reverse transcriptase.Cell communication and signaling : CCS · 2019
    Review
  9. Article
  10. Review
  11. Review
  12. Review
  13. Review
  14. Review
  15. Review
  16. Review
  17. Article
  18. Article
  19. Medical genetics and epigenetics of telomerase.Journal of cellular and molecular medicine · 2011
    Review
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

10 authors at 5 institutions in 4 countries.

A AzouzINSERM UMR-S 1007, Paris, France.
Y-L Wu
J Hillion
I Tarkanyi
A Karniguian
J Aradi
M Lanotte
G-Q Chen
M Chehna
E Ségal-Bendirdjian
Université Paris Cité · FRInserm · FRShanghai Jiao Tong University · CNUniversity of Debrecen · HUUniversity of Aleppo · SY

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The expression of hTERT gene, encoding the catalytic subunit of telomerase, is a feature of most cancer cells. Changes in the chromatin environment of its promoter and binding of transcriptional factors have been reported in differentiating cells when its transcription is repressed. However, it is not clear whether these changes are directly involved in this repression or only linked to differentiation. In a maturation-resistant acute promyelocytic leukemia (APL) cell line (NB4-LR1), we have previously identified a new pathway of retinoid-induced hTERT repression independent of differentiation. Using a variant of this cell line (NB4-LR1(SFD)), which resists to this repression, we show that although distinct patterns of histone modifications and transcription factor binding at the proximal domain of hTERT gene promoter could concur to modulate its expression, this region is not sufficient to the on/off switch of hTERT by retinoids. DNA methylation analysis of the hTERT promoter led to the identification of two distinct functional domains, a proximal one, fully unmethylated in both cell lines, and a distal one, significantly methylated in NB4-LR1(SFD) cells, whose methylation was further re-enforced by retinoid treatment. Interestingly, we showed that the binding to this distal domain of a known hTERT repressor, WT1, was defective only in NB4-LR1(SFD) cells. We propose that epigenetic modifications targeting this distal region could modulate the binding of hTERT repressors and account either for hTERT reactivation and resistance to retinoid-induced hTERT downregulation.

Indexed as

Epigenesis, GeneticPromoter Regions, GeneticAcetylationCCCTC-Binding FactorCell Cycle ProteinsCell Line, TumorCpG IslandsDNA MethylationGenes, mycHistonesHumansLeukemia, Promyelocytic, AcuteNuclear ProteinsRepressor ProteinsRNA Polymerase IISp1 Transcription FactorCCCTC-Binding FactorCell Cycle ProteinsCTCF protein, humanHistonesMAD1L1 protein, humanNuclear ProteinsRepressor ProteinsRNA Polymerase IISp1 Transcription FactorTelomeraseTERT protein, humanTretinoin

Identifiers

PMID20072159
OpenAlexW2140933460

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.