Evidence map›Paper›PMID 31216925›Full record

ArticleEpigenetics2019

EZH2 upregulates the PI3K/AKT pathway through IGF1R and MYC in clinically aggressive chronic lymphocytic leukaemia.

Subazini Thankaswamy Kosalai, Mohammad Hamdy Abdelrazak Morsy, Nikos Papakonstantinou, Larry Mansouri, Niki Stavroyianni, Chandrasekhar Kanduri, Kostas Stamatopoulos, Richard Rosenquist, Meena Kanduri

Open access · hybridAbstract read
In one paragraph

Article in Epigenetics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

21 citing papers in PubMed, 31 citations in OpenAlex.

  1. c-Medical sciences (Basel, Switzerland) · 2026
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  9. International journal of molecular sciences · 2023
    Article
  10. The roles of EZH2 in cancer and its inhibitors.Medical oncology (Northwood, London, England) · 2023
    Review
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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 5 institutions in 2 countries.

Subazini Thankaswamy KosalaiDepartment of Medical Biochemistry and Cell Biology, Institute of Biomedicine, Sahlgrenska Academy, University of Gothenburg , Gothenburg , Sweden.
Mohammad Hamdy Abdelrazak MorsyDepartment of Clinical chemistry and Transfusion medicine, Sahlgrenska University Hospital , Gothenburg , Sweden.
Nikos PapakonstantinouInstitute of Applied Biosciences, Center for Research and Technology Hellas , Thessaloniki , Greece.
Larry MansouriDepartment of Molecular Medicine and Surgery, Karolinska Institutet , Stockholm , Sweden.
Niki StavroyianniHematology Department and HCT Unit, G. Papanicolaou Hospital , Thessaloniki , Greece.
Chandrasekhar KanduriDepartment of Medical Biochemistry and Cell Biology, Institute of Biomedicine, Sahlgrenska Academy, University of Gothenburg , Gothenburg , Sweden.
Kostas StamatopoulosInstitute of Applied Biosciences, Center for Research and Technology Hellas , Thessaloniki , Greece.
Richard RosenquistDepartment of Molecular Medicine and Surgery, Karolinska Institutet , Stockholm , Sweden.
Meena KanduriDepartment of Clinical chemistry and Transfusion medicine, Sahlgrenska University Hospital , Gothenburg , Sweden.
Centre for Research and Technology Hellas · GRKarolinska Institutet · SESahlgrenska University Hospital · SEUniversity of Gothenburg · SEG. Papanikolaou General Hospital · GR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

EZH2 is overexpressed in poor-prognostic chronic lymphocytic leukaemia (CLL) cases, acting as an oncogene; however, thus far, the EZH2 target genes in CLL have not been disclosed. In this study, using ChIP-sequencing, we identified EZH2 and H3K27me3 target genes in two prognostic subgroups of CLL with distinct prognosis and outcome, i.e., cases with unmutated (U-CLL, n = 6) or mutated IGHV genes (M-CLL, n = 6). While the majority of oncogenic pathways were equally enriched for EZH2 target genes in both prognostic subgroups, PI3K pathway genes were differentially bound by EZH2 in U-CLL versus M-CLL. The occupancy of EZH2 for selected PI3K pathway target genes was validated in additional CLL samples (n = 16) and CLL cell lines using siRNA-mediated EZH2 downregulation and ChIP assays. Intriguingly, we found that EZH2 directly binds to the

Indexed as

Gene Expression Regulation, NeoplasticSignal TransductionCell Line, TumorEnhancer of Zeste Homolog 2 ProteinHumansLeukemia, LymphoidPhosphatidylinositol 3-KinasesPromoter Regions, GeneticProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-mycReceptor, IGF Type 1Up-RegulationEnhancer of Zeste Homolog 2 ProteinEZH2 protein, humanIGF1R protein, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-mycReceptor, IGF Type 1ChIP sequencingChronic lymphocytic leukemiaEZH2IGFR1PI3K pathway

Identifiers

PMID31216925
PMCPMC6773411
OpenAlexW2949753513

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.