Evidence map›Paper›PMID 22106282›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2011

Role of checkpoint kinase 1 (Chk1) in the mechanisms of resistance to histone deacetylase inhibitors.

Ju-Hee Lee, Megan L Choy, Lang Ngo, Gisela Venta-Perez, Paul A Marks

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

27 citing papers in PubMed, 51 citations in OpenAlex.

  1. Article
  2. Article
  3. The anticancer effects of Aronia berry extract are mediated by Chk1 and p53 in colorectal cancer.Phytomedicine : international journal of phytotherapy and phytopharmacology · 2024
    Article
  4. Article
  5. Article
  6. Article
  7. The contributing factors of resistance or sensitivity to epigenetic drugs in the treatment of AML.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2022
    Review
  8. CD138Aging · 2020
    Article
  9. Article
  10. The Roles of Histone Deacetylases and Their Inhibitors in Cancer Therapy.Frontiers in cell and developmental biology · 2020
    Review
  11. Article
  12. Article
  13. ATR/CHK1 inhibitors and cancer therapy.Radiotherapy and oncology : journal of the European Society for Therapeutic Radiology and Oncology · 2018
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Stability of XIST repression in relation to genomic imprinting following global genome demethylation in a human cell line.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2014
    Article
  19. Article
  20. Article
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 2 institutions in 1 country.

Ju-Hee LeeCell Biology Program, Sloan-Kettering Institute, Memorial Sloan-Kettering Cancer Center, New York, NY 10065, USA.
Megan L Choy
Lang Ngo
Gisela Venta-Perez
Paul A Marks
Memorial Sloan Kettering Cancer Center · USScripps Research Institute · US

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Nicholas D Socci · 1985 to 2026
$347.4M
NCI NIH HHS P30 CA008748NCI NIH HHS P30CA08748-44
6 · The paper itself

Abstract

Histone deacetylase inhibitors (HDACi) are a new group of anticancer drugs with tumor selective toxicity. Normal cells are relatively resistant to HDACi-induced cell death compared with cancer cells. Previously, we found that vorinostat induces DNA breaks in normal and transformed cells, which normal but not cancer cells can repair. In this study, we found that checkpoint kinase 1 (Chk1), a component of the G2 DNA damage checkpoint, is important in the resistance of normal cells to HDACi in vitro and in vivo. Inhibition of Chk1 activity with Chk1 inhibitor (UCN-01, AZD7762, or CHIR-124) in normal cells increases their sensitivity to HDACi (vorinostat, romidepsin, or entinostat) induced cell death, associated with extensive mitotic disruption. Mitotic abnormalities included loss of sister chromatid cohesion and chromosomal disruption. Inhibition of Chk1 did increase HDACi-induced cell death of transformed cells. Thus, Chk1 is an important factor in the resistance of normal cells, and some transformed cells, to HDACi-induced cell death. Use of Chk1 inhibitors in combination with anticancer agents to treat cancers may be associated with substantial toxicity.

Indexed as

Drug ResistanceAnimalsCell Line, TumorCells, CulturedCell SurvivalCheckpoint Kinase 1DNA DamageFibroblastsForeskinHistone Deacetylase InhibitorsHistonesHumansHydroxamic AcidsImmunoblottingMaleMice3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide7-hydroxystaurosporineCheckpoint Kinase 1CHEK1 protein, humanChek1 protein, mouseCHIR-124H2AX protein, humanHistone Deacetylase InhibitorsHistonesHydroxamic AcidsProtein KinasesQuinolinesQuinuclidinesStaurosporineThiophenesUreaVorinostat

Identifiers

PMID22106282
PMCPMC3241758
OpenAlexW2018750602

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.