Evidence map›Paper›PMID 23939379›Full record

ArticleMolecular cancer therapeutics2013

Histone deacetylase regulation of ATM-mediated DNA damage signaling.

K Ted Thurn, Scott Thomas, Paromita Raha, Ian Qureshi, Pamela N Munster

Open access · bronzeAbstract read
In one paragraph

Article in Molecular cancer therapeutics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed
4.3field-weighted citation impact, top 5% 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

75 citing papers in PubMed, 108 citations in OpenAlex.

  1. DNA-Repair Defects and Olaparib in Metastatic Prostate Cancer.The New England journal of medicine · 2015
    Trial
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Getting the right combination to break the epigenetic code.Nature reviews. Clinical oncology · 2025
    Review
  8. Article
  9. Mechanisms of HDACs in cancer development.Frontiers in immunology · 2025
    Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. Review
  18. Article
  19. Article
  20. Article

15 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

5 authors at 1 institution in 1 country.

K Ted ThurnCorresponding Author: Pamela N. Munster, Division of Hematology and Oncology, Department of Medicine, University of California, 1600 Divisadero, Room A719, Box 1711, San Francisco, CA 94143. pmunster@medicine.ucsf.edu.
Scott Thomas
Paromita Raha
Ian Qureshi
Pamela N Munster
University of California, San Francisco · US

Funding

The role of HDAC2 in hormone therapy resistanceR01CA152989 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI MUNSTER, PAMELA N. · 2011 to 2015
$1.6M
The Role of Selective HDAC Enzymes in Drug SensitivityR01CA122657 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI MUNSTER, PAMELA N. · 2007 to 2010
$1.1M
NCI NIH HHS R01 CA122657NCI NIH HHS R01 CA122657-01NCI NIH HHS R01 CA152989
6 · The paper itself

Abstract

Ataxia-telangiectasia mutated (ATM) is a major regulator of the DNA damage response. ATM promotes the activation of BRCA1, CHK2, and p53 leading to the induction of response genes such as CDKN1A (p21), GADD45A, and RRM2B that promote cell-cycle arrest and DNA repair. The upregulation of these response genes may contribute to resistance of cancer cells to genotoxic therapies. Here, we show that histone deacetylases (HDAC) play a major role in mitigating the response of the ATM pathway to DNA damage. HDAC inhibition decreased ATM activation and expression, and attenuated the activation of p53 in vitro and in vivo. Select depletion of HDAC1 and HDAC2 was sufficient to modulate ATM activation, reduce GADD45A and RRM2B induction, and increase sensitivity to DNA strand breaks. The regulation of ATM by HDAC enzymes therefore suggests a vital role for HDAC1 and HDAC2 in the DNA damage response, and the potential use of the ATM pathway as a pharmacodynamic marker for combination therapies involving HDAC inhibitors.

Indexed as

Ataxia Telangiectasia Mutated ProteinsBRCA1 ProteinCheckpoint Kinase 2DNA DamageGene Expression Regulation, NeoplasticHistone Deacetylase 1Histone Deacetylase 2HumansNeoplasmsSignal TransductionTumor Suppressor Protein p53Ataxia Telangiectasia Mutated ProteinsATM protein, humanBRCA1 ProteinBRCA1 protein, humanCheckpoint Kinase 2CHEK2 protein, humanHDAC1 protein, humanHDAC2 protein, humanHistone Deacetylase 1Histone Deacetylase 2TP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID23939379
PMCPMC3821775
OpenAlexW2157174734

What OpenQuestion holds

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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.