Evidence map›Paper›PMID 18778722›Full record

ReviewMutation research2008

DNA methylation in development and human disease.

Suhasni Gopalakrishnan, Beth O Van Emburgh, Keith D Robertson

Registry-linked trialOpen access · greenAbstract readReview
In one paragraph

Review in Mutation research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05306002 (Effects of a Nutritional Intervention in DNA Damage of Patients With Hereditary Breast and Ovarian Cancer Syndrome), which is not on this map. Cited by 112 papers.

0numbers the graph read from it
0cells of the map it votes in
112citing papers in PubMed
9.0field-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.

NCT05306002 nacompletednot on this mapstarted 2017, after this paper: background citation

Effects of a Nutritional Intervention in DNA Damage of Patients With Hereditary Breast and Ovarian Cancer Syndrome

TypeinterventionalSponsorInstituto de Seguridad y Servicios Sociales de los Trabajadores del EstadoRan2017 to 2022Enrolled34ConditionsHBOC Syndrome, DNA Damage, Nutrition TherapyArmsAntioxidant therapy
3 · Its place in the literature

Who cites it

112 citing papers in PubMed, 266 citations in OpenAlex.

  1. Trial
  2. Article
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  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Epigenetic Regulation of EMP/EMT-Dependent Fibrosis.International journal of molecular sciences · 2024
    Review
  13. Article
  14. Consideration of SHP-1 as a Molecular Target for Tumor Therapy.International journal of molecular sciences · 2023
    Review
  15. Article
  16. Review
  17. Review
  18. Article
  19. Article
  20. Article

52 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 2 institutions in 1 country.

Suhasni GopalakrishnanDepartment of Biochemistry & Molecular Biology, University of Florida, Gainesville, FL 32610, USA.
Beth O Van Emburgh
Keith D Robertson
Florida College · USUniversity of Florida · US

Funding

De novo methyltransferase function in chromatin &cancerR01CA114229 · NCI · UNIVERSITY OF FLORIDA · PI ROBERTSON, KEITH D · 2005 to 2017
$3.3M
DNA Methyltransferase Inhibition by Intercalating AgentsR01CA116028 · NCI · UNIVERSITY OF FLORIDA · PI ROBERTSON, KEITH D · 2006 to 2010
$964k
Novel Effects of DNA Intercalators: Inhibition of Epigenetic ModificationsF32CA132327 · NCI · UNIVERSITY OF FLORIDA · PI VAN EMBURGH, BETH O · 2008 to 2009
$97k
NCI NIH HHS F32CA132327NCI NIH HHS R01 CA114229NCI NIH HHS R01CA114229NCI NIH HHS R01 CA116028NCI NIH HHS R01CA116028
6 · The paper itself

Abstract

DNA methylation is a heritable and stable epigenetic mark associated with transcriptional repression. Changes in the patterns and levels of global and regional DNA methylation regulate development and contribute directly to disease states such as cancer. Recent findings provide intriguing insights into the epigenetic crosstalk between DNA methylation, histone modifications, and small interfering RNAs in the control of cell development and carcinogenesis. In this review, we summarize the recent studies in DNA methylation primarily focusing on the interplay between different epigenetic modifications and their potential role in gene silencing in development and disease. Although the molecular mechanisms involved in the epigenetic crosstalk are not fully understood, unraveling their precise regulation is important not only for understanding the underpinnings of cellular development and cancer, but also for the design of clinically relevant and efficient therapeutics using stem cells and anticancer drugs that target tumor initiating cells.

Indexed as

DNA MethylationAnimalsCell DifferentiationEpigenesis, GeneticGene SilencingGrowth and DevelopmentHumansModels, GeneticNeoplasmsPluripotent Stem CellsPolycomb-Group ProteinsRepressor ProteinsPolycomb-Group ProteinsRepressor Proteins

Identifiers

PMID18778722
PMCPMC2647981
OpenAlexW1989573122

What OpenQuestion holds

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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.