Evidence map›Paper›PMID 24145353›Full record

ReviewCancer research2013

Decoding the histone code: Role of H3K36me3 in mismatch repair and implications for cancer susceptibility and therapy.

Guo-Min Li

Open access · bronzeAbstract readReview
In one paragraph

Review in Cancer research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.8field-weighted citation impact, top 10% 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

23 citing papers in PubMed, 42 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. DNA Repair in Nucleosomes: Insights from Histone Modifications and Mutants.International journal of molecular sciences · 2024
    Review
  5. Article
  6. Article
  7. Review
  8. Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. The relation of microsatellite instability to expression of hTERT in human gastric carcinoma.International journal of clinical and experimental pathology · 2019
    Article
  15. Review
  16. Histone Lysine Methylation and Neurodevelopmental Disorders.International journal of molecular sciences · 2017
    Review
  17. Article
  18. Review
  19. ROBO1 deletion as a novel germline alteration in breast and colorectal cancer patients.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
  20. Review
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 2 countries.

Guo-Min LiAuthor's Affiliations: Graduate Center for Toxicology, Markey Cancer Center, University of Kentucky College of Medicine, Lexington, Kentucky; and Tsinghua University School of Medicine, Beijing, China.
Markey Cancer Center · US

Funding

Novel Mechanism of Genome Instability in Colorectal CancerR01CA167181 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI GU, LIYA, LI, GUO-MIN · 2013 to 2017
$1.6M
DNA repair mechanisms in trinucleotide repeat instabilityR01GM089684 · NIGMS · UNIVERSITY OF SOUTHERN CALIFORNIA · PI LI, GUO-MIN · 2010 to 2013
$1.2M
Dissection and Reconstitution of Human Mismatch RepairR01GM072756 · NIGMS · UNIVERSITY OF KENTUCKY · PI LI, GUO-MIN · 2006 to 2009
$1.0M
NCI NIH HHS CA167181NCI NIH HHS R01 CA167181NIGMS NIH HHS GM089684NIGMS NIH HHS R01 GM072756NIGMS NIH HHS R01 GM089684
6 · The paper itself

Abstract

DNA mismatch repair (MMR) maintains genome stability primarily by correcting replication-associated mismatches. Defects in MMR lead to several human cancers characterized by frequent alterations in simple repetitive DNA sequences, a phenomenon called microsatellite instability (MSI). In most MSI-positive cancers, genetic or epigenetic changes that alter the function or expression of an essential MMR protein have been identified. However, in a subset of MSI-positive cancers, epigenetic or genetic changes have not been found in known MMR genes, such that the molecular basis of the MMR defect in these cells remains unknown. A possible answer to this puzzle emerged recently when it was discovered that H3K36me3, a well-studied posttranslational histone modification or histone mark, plays a role in regulating human MMR in vivo. In this review, potential roles for this histone mark to modulate genome stability and cancer susceptibility in human cells are discussed.

Indexed as

Histone CodeBase Pair MismatchHumansLysineMethylationNeoplasmsPolycomb Repressive Complex 2LysinePolycomb Repressive Complex 2

Identifiers

PMID24145353
PMCPMC3818394
OpenAlexW2145090935

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.