Evidence map›Paper›PMID 22956494›Full record

ReviewAdvances in experimental medicine and biology2013

DNA methyltransferases, DNA damage repair, and cancer.

Bilian Jin, Keith D Robertson

Open access · greenAbstract readReview
In one paragraph

Review in Advances in experimental medicine and biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 255 papers.

0numbers the graph read from it
0cells of the map it votes in
255citing papers in PubMed
46.9field-weighted citation impact, top 1% 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

255 citing papers in PubMed, 502 citations in OpenAlex.

  1. Trial
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  5. Review
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  9. Epidrugs in cancer: mechanisms, applications, and future direction.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
    Review
  10. Curcumin in High Doses Reverses the UV-B-InducedPharmaceuticals (Basel, Switzerland) · 2026
    Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Review
  16. Review
  17. Elucidation of theFrontiers in plant science · 2026
    Article
  18. Review
  19. Article
  20. Review

195 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

2 authors at 1 institution in 1 country.

Bilian JinDepartment of Biochemistry and Molecular Biology, Georgia Health Sciences University Cancer Center, CN-2151, 1410 Laney Walker Blvd, Augusta, GA 30912, USA.
Keith D Robertson
Augusta University Health · US

Funding

De novo methyltransferase function in chromatin &cancerR01CA114229 · NCI · UNIVERSITY OF FLORIDA · PI ROBERTSON, KEITH D · 2005 to 2017
$3.3M
Developmental pathways, environmental agents, and epigenetics in liver diseaseR01AA019976 · NIAAA · MAYO CLINIC ROCHESTER · PI LIU, CHEN, ROBERTSON, KEITH D · 2011 to 2015
$3.0M
DNA Methyltransferase Inhibition by Intercalating AgentsR01CA116028 · NCI · UNIVERSITY OF FLORIDA · PI ROBERTSON, KEITH D · 2006 to 2010
$964k
NCI NIH HHS R01 CA114229NCI NIH HHS R01CA114229NCI NIH HHS R01 CA116028NCI NIH HHS R01CA116028NIAAA NIH HHS R01 AA019976
6 · The paper itself

Abstract

The maintenance DNA methyltransferase (DNMT) 1 and the de novo methyltransferases DNMT3A and DNMT3B are all essential for mammalian development. DNA methylation, catalyzed by the DNMTs, plays an important role in maintaining genome stability. Aberrant expression of DNMTs and disruption of DNA methylation patterns are closely associated with many forms of cancer, although the exact mechanisms underlying this link remain elusive. DNA damage repair systems have evolved to act as a genome-wide surveillance mechanism to maintain chromosome integrity by recognizing and repairing both exogenous and endogenous DNA insults. Impairment of these systems gives rise to mutations and directly contributes to tumorigenesis. Evidence is mounting for a direct link between DNMTs, DNA methylation, and DNA damage repair systems, which provide new insight into the development of cancer. Like tumor suppressor genes, an array of DNA repair genes frequently sustain promoter hypermethylation in a variety of tumors. In addition, DNMT1, but not the DNMT3s, appear to function coordinately with DNA damage repair pathways to protect cells from sustaining mutagenic events, which is very likely through a DNA methylation-independent mechanism. This chapter is focused on reviewing the links between DNA methylation and the DNA damage response.

Indexed as

AnimalsDNA DamageDNA MethylationDNA Modification MethylasesDNA RepairHumansNeoplasmsDNA Modification Methylases

Identifiers

PMID22956494
PMCPMC3707278
OpenAlexW206344101

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.