Evidence map›Paper›PMID 31649131›Full record

ArticleHaematologica2020

EVI1 triggers metabolic reprogramming associated with leukemogenesis and increases sensitivity to L-asparaginase.

Yusuke Saito, Daisuke Sawa, Mariko Kinoshita, Ai Yamada, Sachiyo Kamimura, Akira Suekane, Honami Ogoh, Hidemasa Matsuo, Souichi Adachi, Takashi Taga and 5 more

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 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing 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

18 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Blockade of TIGAR prevents CD8Cancer immunology, immunotherapy : CII · 2025
    Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. 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

15 authors at 6 institutions in 3 countries.

Yusuke SaitoDivision of Pediatrics, Faculty of Medicine, University of Miyazaki, Miyazaki.
Daisuke SawaDivision of Pediatrics, Faculty of Medicine, University of Miyazaki, Miyazaki.
Mariko KinoshitaDivision of Pediatrics, Faculty of Medicine, University of Miyazaki, Miyazaki.
Ai YamadaDivision of Pediatrics, Faculty of Medicine, University of Miyazaki, Miyazaki.
Sachiyo KamimuraDivision of Pediatrics, Faculty of Medicine, University of Miyazaki, Miyazaki.
Akira SuekaneDivision of Tumor and Cellular Biochemistry, University of Miyazaki, Miyazaki.
Honami OgohDivision of Tumor and Cellular Biochemistry, University of Miyazaki, Miyazaki.
Hidemasa MatsuoDepartment of Human Health Science, Kyoto University, Kyoto.
Souichi AdachiDepartment of Human Health Science, Kyoto University, Kyoto.
Takashi TagaDepartment of Pediatrics, Shiga University of Medical Science, Shiga.
Daisuke TomizawaDivision of Leukemia and Lymphoma, Children's Cancer Center, National Center for Child Health and Development, Tokyo.
Motomi OsatoCancer Science Institute, National University of Singapore, Singapore.
Tomoyoshi SogaInstitute for Advanced Biosciences, Keio University, Yamagata, Japan.
Kazuhiro MorishitaDivision of Tumor and Cellular Biochemistry, University of Miyazaki, Miyazaki.
Hiroshi MoritakeDivision of Pediatrics, Faculty of Medicine, University of Miyazaki, Miyazaki hiroshi_moritake@med.miyazaki-u.ac.jp.
University of Miyazaki · JPKyoto University · JPChildren's Cancer Center · USKeio University · JPNational University of Singapore · SGShiga University of Medical Science · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Metabolic reprogramming of leukemia cells is important for survival, proliferation, and drug resistance under conditions of metabolic stress in the bone marrow. Deregulation of cellular metabolism, leading to development of leukemia, occurs through abnormally high expression of transcription factors such as MYC and Ecotropic Virus Integration site 1 protein homolog (EVI1). Overexpression of EVI1 in adults and children with mixed lineage leukemia-rearrangement acute myeloid leukemia (MLL-r AML) has a very poor prognosis. To identify a metabolic inhibitor for EVI1-induced metabolic reprogramming in MLL-r AML, we used an XFp extracellular flux analyzer to examine metabolic changes during leukemia development in mouse models of AML expressing MLL-AF9 and Evi1 (Evi1/MF9). Oxidative phosphorylation (OXPHOS) in Evi1/MF9 AML cells accelerated prior to activation of glycolysis, with a higher dependency on glutamine as an energy source. Furthermore, EVI1 played a role in glycolysis as well as driving production of metabolites in the tricarboxylic acid cycle. L-asparaginase (L-asp) exacerbated growth inhibition induced by glutamine starvation and suppressed OXPHOS and proliferation of Evi1/MF9 both

Indexed as

Leukemia, Myeloid, AcuteProto-OncogenesAdultAsparaginaseDNA-Binding ProteinsHumansMDS1 and EVI1 Complex Locus ProteinTranscription FactorsAsparaginaseDNA-Binding ProteinsMDS1 and EVI1 Complex Locus ProteinMECOM protein, humanTranscription Factors

Identifiers

PMID31649131
PMCPMC7395283
OpenAlexW2981560800

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.