Evidence map›Paper›PMID 21146531›Full record

ReviewFEBS letters2011

Dissecting DNA hypermethylation in cancer.

Marcos R H Estécio, Jean-Pierre J Issa

Open access · hybridAbstract readReview
In one paragraph

Review in FEBS letters, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed, 1 pooled it
3.7field-weighted citation impact, top 6% 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

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

  1. Pooled it
  2. Trial
  3. Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Implications of Cellular Mechanical Memory in Bioengineering.ACS biomaterials science & engineering · 2023
    Review
  9. Article
  10. Systematic pan-cancer analysis identifiesAnnals of translational medicine · 2023
    Article
  11. Review
  12. Review
  13. Epigenetic Changes and Functions in Pneumoconiosis.Oxidative medicine and cellular longevity · 2022
    Review
  14. Article
  15. Review
  16. Review
  17. Article
  18. Review
  19. Review
  20. 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

2 authors at 1 institution in 1 country.

Marcos R H EstécioDepartment of Leukemia, UT MD Anderson Cancer Center, Houston, TX 77030, United States. mestecio@mdanderson.org
Jean-Pierre J Issa
The University of Texas MD Anderson Cancer Center · US

Funding

University of Texas M.D. Anderson Cancer SPORE-LeukemiaP50CA100632 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI KONOPLEVA, MARINA Y · 2003 to 2023
$43.7M
NCI NIH HHS P50 CA100632
6 · The paper itself

Abstract

There is compelling evidence to support the importance of DNA methylation alterations in cancer development. Both losses and gains of DNA methylation are observed, thought to contribute pathophysiologically by inactivating tumor suppressor genes, inducing chromosomal instability and ectopically activating gene expression. Lesser known are the causes of aberrant DNA methylation. Recent studies have pointed out that intrinsic gene susceptibility to DNA methylation, environmental factors and gene function all have an intertwined participation in this process. Overall, these data support a deterministic rather than a stochastic mechanism for de novo DNA methylation in cancer. In this review article, we discuss the technologies available to study DNA methylation and the endogenous and exogenous factors that influence the onset of de novo methylation in cancer.

Indexed as

AnimalsDNA MethylationHumansNeoplasms

Identifiers

PMID21146531
PMCPMC3378045
OpenAlexW2142139678

What OpenQuestion holds

Textmetadata
LicenceTDM
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.