Evidence map›Paper›PMID 24292681›Full record

ArticleOncogene2014

The role of p21(waf1/cip1) and p27(Kip1) in HDACi-mediated tumor cell death and cell cycle arrest in the Eμ-myc model of B-cell lymphoma.

A Newbold, J M Salmon, B P Martin, K Stanley, R W Johnstone

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

32 citing papers in PubMed, 49 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Genome instability and lymphoma.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2021
    Article
  7. Tau Stabilizes Chromatin Compaction.Frontiers in cell and developmental biology · 2021
    Article
  8. The Roles of Histone Deacetylases and Their Inhibitors in Cancer Therapy.Frontiers in cell and developmental biology · 2020
    Review
  9. Article
  10. Cross-talk between Myc and p53 in B-cell lymphomas.Chronic diseases and translational medicine · 2019
    Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  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.

A NewboldCancer Therapeutics Program, Gene Regulation Laboratory, The Peter MacCallum Cancer Institute, St Andrews Place, East Melbourne, Victoria, Australia.
J M SalmonCancer Therapeutics Program, Gene Regulation Laboratory, The Peter MacCallum Cancer Institute, St Andrews Place, East Melbourne, Victoria, Australia.
B P MartinCancer Therapeutics Program, Gene Regulation Laboratory, The Peter MacCallum Cancer Institute, St Andrews Place, East Melbourne, Victoria, Australia.
K StanleyCancer Therapeutics Program, Gene Regulation Laboratory, The Peter MacCallum Cancer Institute, St Andrews Place, East Melbourne, Victoria, Australia.
R W Johnstone1] Cancer Therapeutics Program, Gene Regulation Laboratory, The Peter MacCallum Cancer Institute, St Andrews Place, East Melbourne, Victoria, Australia [2] The Sir Peter MacCallum Department of Oncology, University of Melbourne, Parkville, Victoria, Australia.
Peter MacCallum Cancer Centre · AUUniversity of Melbourne · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Following the establishment of histone deacetylases (HDACs) as promising therapeutic targets for the reversal of aberrant epigenetic states associated with cancer, the development of HDAC inhibitors (HDACi) and their underlying mechanisms of action has been a significant area of scientific interest. HDACi induce diverse biological responses including the inhibition of cell proliferation by blocking progression through the G1 or G2/M phases of the cell cycle. As a putative tumor-suppressor protein, p21(waf1/cip1) influences cell proliferation by inhibiting the activity of cyclin-cyclin-dependent kinase (CDK) complexes at the G1/S and G2/M cell cycle checkpoints. HDACi transcriptionally activate CDKN1A, and it has been proposed that induction of p21(waf1/cip1) can determine if a cell undergoes apoptosis or cell cycle arrest following HDACi treatment. In the Eμ-myc transgenic mouse model of B-cell lymphoma, knockout of cdkn1a had no effect on disease latency, indicating that p21(waf1/cip1) did not function as a tumor suppressor in this system. Although HDACi robustly induced expression of p21(waf1/cip1) in wild-type Eμ-myc lymphomas, deletion of cdkn1a did not sensitize the lymphoma cells to HDACi-induced apoptosis and HDACi-induced cell cycle arrest still occurred. However, knockdown of cdkn1b in cdkn1a knockout lymphomas resulted in defective vorinostat-mediated arrest at G1/S indicating an essential role of p27(Kip1) in mediating this biological response to vorinostat. These data demonstrate that induction of cdkn1a does not regulate HDACi-mediated tumor cell apoptosis and refute the notion that p21(waf1/cip1) is an obligate mediator of HDACi-induced cell cycle arrest.

Indexed as

AnimalsApoptosisCell Cycle CheckpointsCell DeathCyclin-Dependent Kinase Inhibitor p21Cyclin-Dependent Kinase Inhibitor p27Disease Models, AnimalFemaleGene Expression Regulation, NeoplasticGenes, mycGenes, Tumor SuppressorHistone Deacetylase InhibitorsHydroxamic AcidsLymphoma, B-CellMaleMice, KnockoutCdkn1a protein, mouseCdkn1b protein, mouseCyclin-Dependent Kinase Inhibitor p21Cyclin-Dependent Kinase Inhibitor p27Histone Deacetylase InhibitorsHydroxamic AcidsVorinostat

Identifiers

PMID24292681
OpenAlexW2087872121

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.