Evidence map›Paper›PMID 20495664›Full record

ReviewEpigenomics2009

DNA hypomethylation in cancer cells.

Melanie Ehrlich

2 registry-linked trialsOpen access · greenAbstract readReview
In one paragraph

Review in Epigenomics, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to 2 registered trials, which are not on this map. Cited by 586 papers.

0numbers the graph read from it
0cells of the map it votes in
586citing papers in PubMed
11.4field-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.

NCT03467178 phase2unknown statusnot on this mapstarted 2018, after this paper: background citation

Randomized Phase II Study on Decitabine Plus Carboplatin Versus Physician's Choice Chemotherapy in Recurrent, Platinum-resistant Ovarian Cancer.

TypeinterventionalSponsorFondazione IRCCS Istituto Nazionale dei Tumori, MilanoRan2018 to 2021Enrolled119ConditionsRecurrent, Platinum-resistant Ovarian CancerArmsDecitabine, Carboplatin, Pegylated Liposomal Doxorubicin, Gemcitabine, Paclitaxel
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

586 citing papers in PubMed, 1,072 citations in OpenAlex.

  1. Article
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  9. Uncovering alterations in cancer epigenetics via trans-dimensional Markov chain Monte Carlo and hidden Markov models.Journal of the Royal Statistical Society. Series C, Applied statistics · 2026
    Article
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  14. Review
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  16. Toward the simultaneous detection of multiple diseases with a highly cost-effective cell-free DNA methylome test.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
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  18. Review
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526 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

1 author at 1 institution in 1 country.

Melanie EhrlichHayward Genetics Program, Department of Biochemistry, Tulane Cancer Center, Tulane Medical School, 1430 TulaneAvenue, New Orleans, LA 70112, USA. ehrlich@tulane.edu
Tulane Medical Center · US

Funding

FSHD: Chromatin Structure, Looping, &ExpressionR01NS048859 · NINDS · TULANE UNIVERSITY OF LOUISIANA · PI EHRLICH, MELANIE E · 2004 to 2009
$2.0M
NINDS NIH HHS R01 NS048859
6 · The paper itself

Abstract

DNA hypomethylation was the initial epigenetic abnormality recognized in human tumors. However, for several decades after its independent discovery by two laboratories in 1983, it was often ignored as an unwelcome complication, with almost all of the attention on the hypermethylation of promoters of genes that are silenced in cancers (e.g., tumor-suppressor genes). Because it was subsequently shown that global hypomethylation of DNA in cancer was most closely associated with repeated DNA elements, cancer linked-DNA hypomethylation continued to receive rather little attention. DNA hypomethylation in cancer can no longer be considered an oddity, because recent high-resolution genome-wide studies confirm that DNA hypomethylation is the almost constant companion to hypermethylation of the genome in cancer, just usually (but not always) in different sequences. Methylation changes at individual CpG dyads in cancer can have a high degree of dependence not only on the regional context, but also on neighboring sites. DNA demethylation during carcinogenesis may involve hemimethylated dyads as intermediates, followed by spreading of the loss of methylation on both strands. In this review, active demethylation of DNA and the relationship of cancer-associated DNA hypomethylation to cancer stem cells are discussed. Evidence is accumulating for the biological significance and clinical relevance of DNA hypomethylation in cancer, and for cancer-linked demethylation and de novo methylation being highly dynamic processes.

Indexed as

Models, BiologicalCpG IslandsDNA MethylationEpigenesis, GeneticGene Expression Regulation, NeoplasticHumansNeoplasmsNeoplastic Stem CellscancerDNA methylationDNA repeatsgenomic sequencinghypermethylationhypomethylation

Identifiers

PMID20495664
PMCPMC2873040
OpenAlexW2139077902

What OpenQuestion holds

Textmetadata
LicenceTDM
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.