Evidence map›Paper›PMID 20716667›Full record

ArticleGenome research2010

Genome architecture marked by retrotransposons modulates predisposition to DNA methylation in cancer.

Marcos R H Estécio, Juan Gallegos, Céline Vallot, Ryan J Castoro, Woonbok Chung, Shinji Maegawa, Yasuhiro Oki, Yutaka Kondo, Jaroslav Jelinek, Lanlan Shen and 5 more

Open access · bronzeAbstract read
In one paragraph

Article in Genome research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

51 citing papers in PubMed, 1 synthesis or guideline pooled it, 87 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Computational Methods for Single-cell DNA Methylome Analysis.Genomics, proteomics & bioinformatics · 2023
    Review
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  8. Article
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  19. Article
  20. Direct sensing of 5-methylcytosine by polymerase chain reaction.Angewandte Chemie (International ed. in English) · 2014
    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

15 authors at 5 institutions in 3 countries.

Marcos R H EstécioDepartment of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA. mestecio@mdanderson.org
Juan Gallegos
Céline Vallot
Ryan J Castoro
Woonbok Chung
Shinji Maegawa
Yasuhiro Oki
Yutaka Kondo
Jaroslav Jelinek
Lanlan Shen
Helge Hartung
Peter D Aplan
Bogdan A Czerniak
Shoudan Liang
Jean-Pierre J Issa
The University of Texas MD Anderson Cancer Center · USAichi Cancer Center · JPNational Institutes of Health · USBaylor College of Medicine · USCentre National de la Recherche Scientifique · FR

Funding

University of Texas M.D. Anderson Cancer SPORE-LeukemiaP50CA100632 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI SHPALL, ELIZABETH J · 2003 to 2023
$43.7M
Collaborative Pathways that Lead to LeukemiaZIABC010982 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI APLAN, PETER · 2009 to 2025
$8.7M
Activation of Proto-Oncogenes by Chromosomal TranslocationZIASC010378 · NCI · DIVISION OF CLINICAL SCIENCES - NCI · PI APLAN, PETER · 2009 to 2025
$8.4M
Pre-clinical Studies of Therapy for Myelodysplastic SyndromeZIABC010983 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI APLAN, PETER · 2009 to 2025
$8.2M
EARLY DETECTION OF URINARY BLADDER CANCERU01CA085078 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI CZERNIAK, BOGDAN A · 1999 to 2009
$6.1M
DNA Methylation in Colon Cancer MetastasisR01CA098006 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI ISSA, JEAN-PIERRE J. · 2004 to 2008
$1.4M
Genome-wide Identification of Minor Histocompatibility AntigensK25CA123344 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI LIANG, SHOUDAN · 2008 to 2012
$734k
Intramural NIH HHSNCI NIH HHS K25 CA123344NCI NIH HHS P50 CA100632NCI NIH HHS R01 CA098006NCI NIH HHS U01 CA085078
6 · The paper itself

Abstract

Epigenetic silencing plays an important role in cancer development. An attractive hypothesis is that local DNA features may participate in differential predisposition to gene hypermethylation. We found that, compared with methylation-resistant genes, methylation-prone genes have a lower frequency of SINE and LINE retrotransposons near their transcription start site. In several large testing sets, this distribution was highly predictive of promoter methylation. Genome-wide analysis showed that 22% of human genes were predicted to be methylation-prone in cancer; these tended to be genes that are down-regulated in cancer and that function in developmental processes. Moreover, retrotransposon distribution marks a larger fraction of methylation-prone genes compared to Polycomb group protein (PcG) marking in embryonic stem cells; indeed, PcG marking and our predictive model based on retrotransposon frequency appear to be correlated but also complementary. In summary, our data indicate that retrotransposon elements, which are widespread in our genome, are strongly associated with gene promoter DNA methylation in cancer and may in fact play a role in influencing epigenetic regulation in normal and abnormal physiological states.

Indexed as

DNA MethylationCell Line, TumorEpigenomicsGene Expression Regulation, NeoplasticGene SilencingGenome, HumanHumansLeukemia, Myeloid, AcuteNeoplasmsRetroelementsTumor Cells, CulturedUrinary Bladder NeoplasmsRetroelements

Identifiers

PMID20716667
PMCPMC2945186
OpenAlexW2139946616

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.