Evidence map›Paper›PMID 28720764›Full record

ArticleLeukemia2018

High expression of ABCG2 induced by EZH2 disruption has pivotal roles in MDS pathogenesis.

K C Kawabata, Y Hayashi, D Inoue, H Meguro, H Sakurai, T Fukuyama, Y Tanaka, S Asada, T Fukushima, R Nagase and 7 more

Abstract read
PubMed Publisher
In one paragraph

Article in Leukemia, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.1field-weighted citation impact, top 49% 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

6 citing papers in PubMed, 8 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Multidrug efflux transporter ABCG2: expression and regulation.Cellular and molecular life sciences : CMLS · 2021
    Review
  5. Article
  6. Deciphering the Therapeutic Resistance in Acute Myeloid Leukemia.International journal of molecular sciences · 2020
    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

17 authors at 6 institutions in 2 countries.

K C KawabataDivision of Cellular Therapy, Institute of Medical Science, The University of Tokyo, Minato, Tokyo, Japan.
Y HayashiDivision of Cellular Therapy, Institute of Medical Science, The University of Tokyo, Minato, Tokyo, Japan.
D InoueDivision of Cellular Therapy, Institute of Medical Science, The University of Tokyo, Minato, Tokyo, Japan.
H MeguroLaboratory of Oncology, School of Life Sciences, Tokyo University of Pharmacy and Life Sciences, Hachioji, Japan.
H SakuraiDivision of Hematology, Department of Medicine, Juntendo University, Bunkyo, Japan.
T FukuyamaDivision of Cellular Therapy, Institute of Medical Science, The University of Tokyo, Minato, Tokyo, Japan.
Y TanakaDivision of Cellular Therapy, Institute of Medical Science, The University of Tokyo, Minato, Tokyo, Japan.
S AsadaDivision of Cellular Therapy, Institute of Medical Science, The University of Tokyo, Minato, Tokyo, Japan.
T FukushimaDivision of Cellular Therapy, Institute of Medical Science, The University of Tokyo, Minato, Tokyo, Japan.
R NagaseDivision of Cellular Therapy, Institute of Medical Science, The University of Tokyo, Minato, Tokyo, Japan.
R TakedaDivision of Cellular Therapy, Institute of Medical Science, The University of Tokyo, Minato, Tokyo, Japan.
Y HaradaDivision of Hematology, Department of Medicine, Juntendo University, Bunkyo, Japan.
J KitauraDivision of Cellular Therapy, Institute of Medical Science, The University of Tokyo, Minato, Tokyo, Japan.
S GoyamaDivision of Cellular Therapy, Institute of Medical Science, The University of Tokyo, Minato, Tokyo, Japan.
H HaradaLaboratory of Oncology, School of Life Sciences, Tokyo University of Pharmacy and Life Sciences, Hachioji, Japan.
H AburataniGenome Science Division, Research Center for Advanced Science and Technology, The University of Tokyo, Meguro, Japan.ORCID 0000-0003-0438-1544
T KitamuraDivision of Cellular Therapy, Institute of Medical Science, The University of Tokyo, Minato, Tokyo, Japan.
The University of Tokyo · JPJuntendo University · JPTokyo University of Pharmacy and Life Sciences · JPBunkyo Gakuin University · JPCornell University · USMemorial Sloan Kettering Cancer Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Both proto-oncogenic and tumor-suppressive functions have been reported for enhancer of zeste homolog 2 (EZH2). To investigate the effects of its inactivation, a mutant EZH2 lacking its catalytic domain was prepared (EZH2-dSET). In a mouse bone marrow transplant model, EZH2-dSET expression in bone marrow cells induced a myelodysplastic syndrome (MDS)-like disease in transplanted mice. Analysis of these mice identified Abcg2 as a direct target of EZH2. Intriguingly, Abcg2 expression alone induced the same disease in the transplanted mice, where stemness genes were enriched. Interestingly, ABCG2 expression is specifically high in MDS patients. The present results indicate that ABCG2 de-repression induced by EZH2 mutations have crucial roles in MDS pathogenesis.

Indexed as

AnimalsATP Binding Cassette Transporter, Subfamily G, Member 2Disease Models, AnimalEnhancer of Zeste Homolog 2 ProteinMiceMutationMyelodysplastic SyndromesAbcg2 protein, mouseATP Binding Cassette Transporter, Subfamily G, Member 2Enhancer of Zeste Homolog 2 ProteinEzh2 protein, mouse

Identifiers

PMID28720764
OpenAlexW2737586525

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.