Evidence map›Paper›PMID 19369964›Full record

ArticleLeukemia2009

Enhanced expression of FHL2 leads to abnormal myelopoiesis in vivo.

Z Qian, L Mao, A A Fernald, H Yu, R Luo, Y Jiang, J Anastasi, P J Valk, R Delwel, M M Le Beau

Abstract read
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In one paragraph

Article in Leukemia, 2009. 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
0.9field-weighted citation impact, top 25% 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, 31 citations in OpenAlex.

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  15. Critical role of miR-9 in myelopoiesis and EVI1-induced leukemogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2013
    Article
  16. Article
  17. FHL2 protein is a novel co-repressor of nuclear receptor Nur77.The Journal of biological chemistry · 2011
    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

10 authors at 3 institutions in 2 countries.

Z QianSection of Hematology/Oncology and the Cancer Research Center, University of Chicago, Chicago, IL 60637, USA. zqian@bsd.uchicago.edu
L Mao
A A Fernald
H Yu
R Luo
Y Jiang
J Anastasi
P J Valk
R Delwel
M M Le Beau
Cancer Research Center · USUniversity of Chicago · USErasmus MC · NL

Funding

NCI NIH HHS CA40046
6 · The paper itself

Abstract

FHL2 is a multifunctional LIM domain protein that acts as a transcriptional modulator mediating proliferation and apoptosis in a tissue-specific manner. Upregulation of FHL2 has been detected in a variety of cancers. We demonstrate that upregulation of FHL2 is associated with a subset of acute myeloid leukemia with a characteristic gene-expression signature, and abnormalities of chromosome 5. In mice, expression of endogenous Fhl2 is downregulated coordinately during the differentiation of hematopoietic cells. Upregulation of FHL2 enhances proliferation of myeloid progenitor cells, and serial-replating efficiency of hematopoietic cells in vitro. Chimeric mice with enforced expression of FHL2 in bone marrow cells, are characterized by an expanded pool of myeloid progenitor cells, enhanced granulopoiesis and megakaryocytopoiesis. In addition, enhanced expression of FHL2 promotes cell-cycle entry of myeloid progenitor cells and increases the frequency of apoptosis of bone marrow cells in vivo. These results raise the possibility that deregulation of FHL2 contributes to the development of human myeloid disorders.

Indexed as

MyelopoiesisAnimalsCell ProliferationHematopoiesisHomeodomain ProteinsLeukemia, Myeloid, AcuteLIM-Homeodomain ProteinsMaleMiceMice, Inbred BALB CMice, Inbred C57BLMuscle ProteinsMyeloid Progenitor CellsThrombopoiesisTranscription FactorsFhl2 protein, mouseHomeodomain ProteinsLIM-Homeodomain ProteinsMuscle ProteinsTranscription Factors

Identifiers

PMID19369964
OpenAlexW2060681477

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.