Evidence map›Paper›PMID 27617578›Full record

ArticleOncogene2017

Upregulation of Flt3 is a passive event in Hoxa9/Meis1-induced acute myeloid leukemia in mice.

A Staffas, L S Arabanian, S Y Wei, A Jansson, S Ståhlman, P Johansson, L Fogelstrand, J Cammenga, F Kuchenbauer, L Palmqvist

Abstract read
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In one paragraph

Article in Oncogene, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
–field-weighted citation impact
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

14 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Article
  6. Open biology · 2022
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Oncogenic and tumor suppressor function of MEIS and associated factors.Turkish journal of biology = Turk biyoloji dergisi · 2020
    Article
  13. Article
  14. 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.

A StaffasDepartment of Clinical Chemistry and Transfusion Medicine, Institute of Biomedicine, University of Gothenburg, Gothenburg, Sweden.
L S ArabanianDepartment of Clinical Chemistry and Transfusion Medicine, Institute of Biomedicine, University of Gothenburg, Gothenburg, Sweden.
S Y WeiDepartment of Clinical Chemistry and Transfusion Medicine, Institute of Biomedicine, University of Gothenburg, Gothenburg, Sweden.
A JanssonDepartment of Clinical Chemistry, Sahlgrenska University Hospital, Gothenburg, Sweden.
S StåhlmanDepartment of Clinical Chemistry and Transfusion Medicine, Institute of Biomedicine, University of Gothenburg, Gothenburg, Sweden.
P JohanssonDepartment of Clinical Chemistry and Transfusion Medicine, Institute of Biomedicine, University of Gothenburg, Gothenburg, Sweden.
L FogelstrandDepartment of Clinical Chemistry and Transfusion Medicine, Institute of Biomedicine, University of Gothenburg, Gothenburg, Sweden.
J CammengaDepartment of Clinical and Experimental Medicine, Linköping University, Linköping, Sweden.
F KuchenbauerDepartment of Internal Medicine III, University Hospital of Ulm, Ulm, Germany.
L PalmqvistDepartment of Clinical Chemistry and Transfusion Medicine, Institute of Biomedicine, University of Gothenburg, Gothenburg, Sweden.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

HOXA9, MEIS1 and FLT3 are genes frequently upregulated in human acute myeloid leukemia. Hoxa9 and Meis1 also cooperate to induce aggressive AML with high Flt3 expression in mice, suggesting an important role for Flt3 in Hoxa9/Meis1-induced leukemogenesis. To define the role of Flt3 in AML with high Hoxa9/Meis1, we treated mice with Hoxa9/Meis1-induced AML with the Flt3 inhibitor AC220, used an Flt3-ligand (FL-/-) knockout model, and investigated whether overexpression of Flt3 could induce leukemia together with overexpression of Hoxa9. Flt3 inhibition by AC220 did not delay AML development in mice transplanted with bone marrow cells overexpressing Hoxa9 and Meis1. In addition, Hoxa9/Meis1 cells induced AML in FL-/- mice as rapid as in wild-type mice. However, FL-/- mice had reduced organ infiltration compared with wild-type mice, suggesting some Flt3-dependent effect on leukemic invasiveness. Interestingly, leukemic Hoxa9/Meis1 cells from sick mice expressed high levels of Flt3 regardless of presence of its ligand, showing that Flt3 is a passive marker on these cells. In line with this, combined engineered overexpression of Flt3 and Hoxa9 did not accelerate the progression to AML. We conclude that the Hoxa9- and Meis1-associated upregulation of Flt3 is not a requirement for leukemic progression induced by Hoxa9 and Meis1.

Indexed as

AnimalsBenzothiazolesBiomarkersCell ProliferationDisease Models, Animalfms-Like Tyrosine Kinase 3Gene ExpressionGene Expression Regulation, LeukemicHomeodomain ProteinsHumansLeukemia, Myeloid, AcuteMiceMice, KnockoutMyeloid Ecotropic Viral Integration Site 1 ProteinNeoplasm ProteinsPhenylurea CompoundsBenzothiazolesBiomarkersfms-Like Tyrosine Kinase 3homeobox protein HOXA9Homeodomain ProteinsMEIS1 protein, humanMeis1 protein, mouseMyeloid Ecotropic Viral Integration Site 1 ProteinNeoplasm ProteinsPhenylurea Compoundsquizartinib

Identifiers

PMID27617578

What OpenQuestion holds

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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.