Evidence map›Paper›PMID 11420732›Full record

ReviewOncogene2001

DNA methylation, chromatin inheritance, and cancer.

M R Rountree, K E Bachman, J G Herman, S B Baylin

Abstract readReview
PubMed Publisher
In one paragraph

Review in Oncogene, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 133 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
133citing papers in PubMed, 2 pooled it
12.0field-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.

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

133 citing papers in PubMed, 2 syntheses or guidelines pooled it, 385 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. The mechanisms and clinical significance of CD8Cancer biology & medicine · 2025
    Review
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  5. Article
  6. Article
  7. Article
  8. Article
  9. Targeted Sequencing Identifies the Genetic Variants Associated with High-altitude Polycythemia in the Tibetan Population.Indian journal of hematology & blood transfusion : an official journal of Indian Society of Hematology and Blood Transfusion · 2022
    Article
  10. Article
  11. Article
  12. Epigenetics in psoriasis: perspective of DNA methylation.Molecular genetics and genomics : MGG · 2021
    Review
  13. Epigenetics in Non-tumor Immune-Mediated Skin Diseases.Molecular diagnosis & therapy · 2021
    Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Regulation ofEpigenetics · 2019
    Article
  20. Article

73 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

4 authors at 2 institutions in 1 country.

M R RountreeThe Johns Hopkins Oncology Center, Tumor Biology Laboratory, The Johns Hopkins University School of Medicine, Baltimore, Maryland, MD 21231, USA.
K E Bachman
J G Herman
S B Baylin
Johns Hopkins University · USJohns Hopkins Medicine · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer is a process driven by the accumulation of abnormalities in gene function. While many of these changes are genetic, epigenetically mediated changes in gene expression are being increasingly appreciated. This latter process emphasizes the need to understand two key components of heritable, but reversible, modulation of gene promoter function that are closely tied to one another - formation of chromatin which modulates transcription and establishing patterns of DNA methylation. The link lies first in the recruitment to methylated cytosines of a family of methyl-CpG binding domain proteins (MBDs), which are direct transcriptional repressors and can complex with transcriptional corepressors including histone deacetylases (HDACs). Additionally, the proteins that catalyze DNA methylation, DNA methyltransferases (DNMTs), also directly repress transcription and associate with HDACs. Regulation of these above chromatin-DNA methylation interactions as a function of DNA replication timing is emerging as a key event in the inheritance of transcriptionally repressed domains of the genome. Importantly, synergy between HDAC activity and DNA methylation is operative for a key epigenetic abnormality in cancer cells, transcriptional silencing of tumor suppressor genes. This change has now been recognized for genes that are essential for normal regulation of virtually every major cell function including cell growth, differentiation, apoptosis, DNA repair, and cell-cell, cell-substratum interaction. Understanding the molecular determinants of both normal and abnormal patterns of chromatin formation and DNA methylation thus holds great promise for our understanding of cancer and for means to better diagnose, prevent, and treat this disease.

Indexed as

DNA MethylationAnimalsChromatinDNA, NeoplasmGene Expression Regulation, NeoplasticHumansNeoplasmsTranscription, GeneticChromatinDNA, Neoplasm

Identifiers

PMID11420732
OpenAlexW2324384090

What OpenQuestion holds

Textmetadata
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.