Evidence map›Paper›PMID 19509173›Full record

ArticleClinical cancer research : an official journal of the American Association for Cancer Research2009

Cancer DNA methylation: molecular mechanisms and clinical implications.

Michael T McCabe, Johann C Brandes, Paula M Vertino

Registry-linked trialOpen access · bronzeAbstract read
In one paragraph

Article in Clinical cancer research : an official journal of the American Association for Cancer Research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07126626 (Multi-center Prospective Validation of the SPOT-MAS Lung Test Using Circulating Tumor DNA for the Detection of Lung Cancer), which is not on this map. Cited by 141 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
141citing papers in PubMed, 2 pooled it
9.8field-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.

NCT07126626 not yet recruitingnot on this mapstarted 2025, after this paper: background citation

Multi-center Prospective Validation of the SPOT-MAS Lung Test Using Circulating Tumor DNA for the Detection of Lung Cancer

TypeobservationalSponsorGene SolutionsRan2025 to 2027Enrolled1,184ConditionsLung Diseases, Lung Cancer Screening
3 · Its place in the literature

Who cites it

141 citing papers in PubMed, 2 syntheses or guidelines pooled it, 261 citations in OpenAlex.

  1. A Meta-Analysis of the Association betweenBioMed research international · 2017
    Pooled it
  2. Pooled it
  3. Article
  4. Review
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  6. Review
  7. Article
  8. Maternal O-GlcNAc Transferase Is Required for the Asymmetry of Epigenetic Modifications in Mouse Zygotes.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
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  15. Article
  16. Review
  17. Review
  18. Article
  19. Frontiers in molecular biosciences · 2024
    Article
  20. Article

81 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

3 authors at 1 institution in 1 country.

Michael T McCabeDepartment of Radiation Oncology and Hematology, Emory University School of Medicine and the Emory Winship Cancer Institute, Atlanta, Georgia 30322, USA.
Johann C Brandes
Paula M Vertino
Emory University · US

Funding

Targeting Microtubules and HDAC6 in NSCLCP01CA116676 · NCI · EMORY UNIVERSITY · PI KHURI, FADLO RAJA · 2006 to 2012
$8.0M
GENESIS AND CONSEQUENCES OF ABERRANT DNA METHYLATIONR01CA077337 · NCI · EMORY UNIVERSITY · PI VERTINO, PAULA M. · 1998 to 2016
$3.4M
Defining Genomic Signatures for Aberrant DNA Methylation in Human CancersR01CA132065 · NCI · EMORY UNIVERSITY · PI VERTINO, PAULA M. · 2009 to 2013
$1.5M
NCI NIH HHS P01 CA116676NCI NIH HHS R01 CA077337NCI NIH HHS R01 CA132065
6 · The paper itself

Abstract

DNA methylation plays a crucial role in the regulation of gene expression and chromatin organization within normal eukaryotic cells. In cancer, however, global patterns of DNA methylation are altered with global hypomethylation of repeat-rich intergenic regions and hypermethylation of a subset of CpG-dense gene-associated regions (CpG islands). Extensive research has revealed the cellular machinery that catalyzes DNA methylation, as well as several large protein complexes that mediate the transcriptional repression of hypermethylated genes. However, research is only just beginning to uncover the molecular mechanisms underlying the origins of cancer-specific DNA methylation. Herein, we present several recent advances regarding these mechanisms and discuss the relationship between histone modifications (i.e., H3K4me2/3, H4K16Ac, H3K9me2/3, H3K27me3, H4K20me3), chromatin-modifying enzymes (G9a, EZH2, hMOF, SUV4-20H), and aberrant DNA methylation. Additionally, the role played by inflammation, DNA damage, and miRNAs in the etiology of aberrant DNA methylation is considered. Finally, we discuss the clinical implications of aberrant DNA methylation and the utility of methylated biomarkers in cancer diagnosis and management.

Indexed as

DNA MethylationEpigenesis, GeneticBiomarkers, TumorCarcinogensChromatinCpG IslandsDNA-Binding ProteinsDNA DamageHistonesHumansMicroRNAsNeoplasmsBiomarkers, TumorCarcinogensChromatinDNA-Binding ProteinsHistonesMicroRNAs

Identifiers

PMID19509173
PMCPMC2715155
OpenAlexW2140713688

What OpenQuestion holds

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Read underepoch 390

Registered trials

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.