Evidence map›Paper›PMID 29143813›Full record

ArticleGene therapy2017

SHIP1, but not an AML-derived SHIP1 mutant, suppresses myeloid leukemia growth in a xenotransplantation mouse model.

M Täger, S Horn, E Latuske, P Ehm, M Schaks, M Nalaskowski, B Fehse, W Fiedler, C Stocking, J Wellbrock and 1 more

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Gene therapy, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.7field-weighted citation impact, top 30% 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

10 citing papers in PubMed, 20 citations in OpenAlex.

  1. Review
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  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Strategy for Leukemia Treatment Targeting SHP-1,2 and SHIP.Frontiers in cell and developmental biology · 2021
    Review
  10. 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

11 authors at 2 institutions in 1 country.

M TägerInstitute of Biochemistry and Signal Transduction, Center for Experimental Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
S HornResearch Department Cell and Gene Therapy, Department of Stem Cell Transplantation, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
E LatuskeDepartment of Oncology, Haematology and Bone Marrow Transplantation with section Pneumology, Hubertus Wald University Cancer Center, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
P EhmInstitute of Biochemistry and Signal Transduction, Center for Experimental Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
M SchaksInstitute of Biochemistry and Signal Transduction, Center for Experimental Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
M NalaskowskiInstitute of Biochemistry and Signal Transduction, Center for Experimental Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
B FehseResearch Department Cell and Gene Therapy, Department of Stem Cell Transplantation, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.ORCID 0000-0001-9780-7211
W FiedlerDepartment of Oncology, Haematology and Bone Marrow Transplantation with section Pneumology, Hubertus Wald University Cancer Center, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
C StockingHeinrich-Pette-Institute, Leibniz Institute for Experimental Virology, Molecular Pathology, Hamburg, Germany.
J WellbrockDepartment of Oncology, Haematology and Bone Marrow Transplantation with section Pneumology, Hubertus Wald University Cancer Center, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
M JückerInstitute of Biochemistry and Signal Transduction, Center for Experimental Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Universität Hamburg · DELeibniz Institute of Virology (LIV) · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Constitutive activation of the PI3K/AKT signaling pathway is found in ~50-70% of AML patients. The SH2-containing inositol 5-phosphatase 1 (SHIP1) is a negative regulator of PI3K/AKT signaling in hematopoietic cells. SHIP1 knockout mice develop a myeloproliferative syndrome and concomitant deletion of SHIP1 and the tumor suppressor PTEN leads to the development of lethal B-cell lymphomas. In the study presented here, we investigated the role of SHIP1 as a tumor suppressor in myeloid leukemia cells in an in vivo xenograft transplantation model. NSG Mice transplanted with UKE-1 cells derived from a secondary AML showed a significantly extended lifespan after lentiviral-mediated overexpression of SHIP1 in comparison to the vector control cohort. In contrast, the AML-derived SHIP1

Indexed as

AnimalsCell Line, TumorCell ProliferationDisease Models, AnimalGene Expression Regulation, LeukemicHumansLentivirusLeukemia, Myeloid, AcuteMiceMice, Inbred NODMice, KnockoutPhosphatidylinositol-3,4,5-Trisphosphate 5-PhosphatasesPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSignal TransductionTransplantation, HeterologousINPP5D protein, humanPhosphatidylinositol-3,4,5-Trisphosphate 5-PhosphatasesPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-akt

Identifiers

PMID29143813
OpenAlexW2769207559

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.