Evidence map›Paper›PMID 26046670›Full record

ArticleOncotarget2015

BEX1 acts as a tumor suppressor in acute myeloid leukemia.

Oscar Lindblad, Tianfeng Li, Xianwei Su, Jianmin Sun, Nuzhat N Kabir, Fredrik Levander, Hui Zhao, Gang Lu, Lars Rönnstrand, Julhash U Kazi

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

20 citing papers in PubMed, 27 citations in OpenAlex.

  1. Review
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  11. Oncology letters · 2020
    Article
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  15. Article
  16. Article
  17. BEX2 promotes tumor proliferation in colorectal cancer.International journal of biological sciences · 2017
    Article
  18. Combination of Imatinib Mesylate and AKT Inhibitor Provides Synergistic Effects in Preclinical Study of Gastrointestinal Stromal Tumor.Clinical cancer research : an official journal of the American Association for Cancer Research · 2017
    Article
  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

10 authors at 4 institutions in 3 countries.

Oscar LindbladDivision of Translational Cancer Research, Department of Laboratory Medicine, Lund University, Lund, Sweden.
Tianfeng LiSchool of Biomedical Sciences, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong.
Xianwei SuSchool of Biomedical Sciences, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong.
Jianmin SunDivision of Translational Cancer Research, Department of Laboratory Medicine, Lund University, Lund, Sweden.
Nuzhat N KabirLaboratory of Computational Biochemistry, KN Biomedical Research Institute, Barisal, Bangladesh.
Fredrik LevanderBioinformatics Infrastructure for Life Sciences (BILS), Department of Immunotechnology, Lund University, Lund, Sweden.
Hui ZhaoSchool of Biomedical Sciences, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong.
Gang LuSchool of Biomedical Sciences, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong.
Lars RönnstrandDivision of Translational Cancer Research, Department of Laboratory Medicine, Lund University, Lund, Sweden.
Julhash U KaziDivision of Translational Cancer Research, Department of Laboratory Medicine, Lund University, Lund, Sweden.
Chinese University of Hong Kong · CNLund University · SEUniversity of Barisal · BDSkåne University Hospital · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acute myeloid leukemia (AML) is a heterogeneous disease of the myeloid lineage. About 35% of AML patients carry an oncogenic FLT3 mutant making FLT3 an attractive target for treatment of AML. Major problems in the development of FLT3 inhibitors include lack of specificity, poor response and development of a resistant phenotype upon treatment. Further understanding of FLT3 signaling and discovery of novel regulators will therefore help to determine additional pharmacological targets in FLT3-driven AML. In this report, we identified BEX1 as a novel regulator of oncogenic FLT3-ITD-driven AML. We showed that BEX1 expression was down-regulated in a group of AML patients carrying FLT3-ITD. Loss of BEX1 expression resulted in poor overall survival (hazard ratio, HR = 2.242, p = 0.0011). Overexpression of BEX1 in mouse pro-B and myeloid cells resulted in decreased FLT3-ITD-dependent cell proliferation, colony and tumor formation, and in increased apoptosis in vitro and in vivo. BEX1 localized to the cytosolic compartment of cells and significantly decreased FLT3-ITD-induced AKT phosphorylation without affecting ERK1/2 or STAT5 phosphorylation. Our data suggest that the loss of BEX1 expression in FLT3-ITD driven AML potentiates oncogenic signaling and leads to decreased overall survival of the patients.

Indexed as

Gene Expression Regulation, LeukemicGenes, Tumor SuppressorAnimalsApoptosisCell LineageCell Line, TumorCell ProliferationChlorocebus aethiopsCOS CellsCytosolfms-Like Tyrosine Kinase 3Gene Expression ProfilingHumansLeukemia, Myeloid, AcuteMaleMiceBEX1 protein, humanFLT3 protein, humanfms-Like Tyrosine Kinase 3Nerve Tissue ProteinsAKTAMLapoptosisFLT3FLT3-ITD

Identifiers

PMID26046670
PMCPMC4673273
OpenAlexW1778624565

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Registered trials

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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.