Evidence map›Paper›PMID 31289198›Full record

ArticleHaematologica2020

EZH2 inhibitors abrogate upregulation of trimethylation of H3K27 by CDK9 inhibitors and potentiate its activity against diffuse large B-cell lymphoma.

Shao Xie, Fan Wei, Yi-Ming Sun, Ying-Lei Gao, Lu-Lu Pan, Min-Jia Tan, Shu-Dong Wang, Jian Ding, Yi Chen

Open access · goldAbstract read
In one paragraph

Article in Haematologica, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.3field-weighted citation impact, top 41% 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

8 citing papers in PubMed, 11 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. JMJD family proteins in cancer and inflammation.Signal transduction and targeted therapy · 2022
    Review
  6. Article
  7. Review
  8. The Functions of the Demethylase JMJD3 in Cancer.International journal of molecular sciences · 2021
    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

9 authors at 4 institutions in 2 countries.

Shao XieDivision of Anti-Tumor Pharmacology, State Key Laboratory of Drug Research and Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, China.
Fan WeiDivision of Anti-Tumor Pharmacology, State Key Laboratory of Drug Research and Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, China.
Yi-Ming SunDivision of Anti-Tumor Pharmacology, State Key Laboratory of Drug Research and Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, China.
Ying-Lei GaoDivision of Anti-Tumor Pharmacology, State Key Laboratory of Drug Research and Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, China.
Lu-Lu PanUniversity of Chinese Academy of Sciences, Beijing, China.
Min-Jia TanChemical Proteomics Center, State Key Laboratory of Drug Research, Shanghai Institute of Materia Medica and Chinese Academy of Sciences, Shanghai, China.
Shu-Dong WangCentre for Drug Discovery and Development, School of Pharmacy and Medical Sciences, University of South Australia Cancer Research Institute, Adelaide, Australia.
Jian DingDivision of Anti-Tumor Pharmacology, State Key Laboratory of Drug Research and Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, China jding@simm.ac.cn.
Yi ChenDivision of Anti-Tumor Pharmacology, State Key Laboratory of Drug Research and Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, China ychen@simm.ac.cn.
Chinese Academy of Sciences · CNShanghai Institute of Materia Medica · CNUniversity of Chinese Academy of Sciences · CNUniversity of South Australia · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aberrant expression of CDK9/cyclin T1 has been found in diffuse large B-cell lymphoma (DLBCL), and suggests that CDK9 is a potential therapeutic target for DLBCL. Here, we firstly demonstrated that CDKI-73, a novel cyclin-dependent kinases (CDK) inhibitor, potently blocks CDK9, triggered apoptosis and dramatically repressed DLBCL cell growth owing to CDK9 inhibition. CDK9 inhibitors specifically elevated the trimethylation of H3K27, which we speculate was due to reduced expression of JMJD3/UTX. Considering the important role of the trimethylation of H3K27 in tumor progression, the synergistic effect of the combination therapy of CDK9 inhibitors with EZH2 inhibitors was investigated. EZH2 inhibitors reversed the upregulation of trimethylation of H3K27, and synergistically inhibited DLBCL and other solid tumors growth

Indexed as

Lymphoma, Large B-Cell, DiffuseApoptosisCell Cycle CheckpointsCyclin-Dependent Kinase 9Enhancer of Zeste Homolog 2 ProteinHumansTranscriptional ActivationUp-RegulationCDK9 protein, humanCyclin-Dependent Kinase 9Enhancer of Zeste Homolog 2 ProteinEZH2 protein, human

Identifiers

PMID31289198
PMCPMC7109751
OpenAlexW2957011118

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.