Evidence map›Paper›PMID 25249015›Full record

ArticleLeukemia2015

Grb10 is involved in BCR-ABL-positive leukemia in mice.

A L Illert, C Albers, S Kreutmair, H Leischner, C Peschel, C Miething, J Duyster

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Leukemia, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.6field-weighted citation impact, top 32% 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

11 citing papers in PubMed, 17 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Interception Targets ofCancer prevention research (Philadelphia, Pa.) · 2021
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  9. APC/CCellular and molecular life sciences : CMLS · 2019
    Article
  10. Article
  11. Review
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

7 authors at 4 institutions in 1 country.

A L IllertDepartment of Hematology/Oncology, University Medical Center Freiburg, Freiburg, Germany.
C Albers1] Department of Hematology/Oncology, University Medical Center Freiburg, Freiburg, Germany [2] Department of Internal Medicine III, Klinikum Rechts der Isar, Technical University of Munich, Munich, Germany.
S KreutmairDepartment of Hematology/Oncology, University Medical Center Freiburg, Freiburg, Germany.
H Leischner1] Department of Internal Medicine III, Klinikum Rechts der Isar, Technical University of Munich, Munich, Germany [2] Department of Hematology, Oncology, and Tumor Immunology, HELIOS Klinikum Berlin-Buch, Berlin, Germany.
C PeschelDepartment of Internal Medicine III, Klinikum Rechts der Isar, Technical University of Munich, Munich, Germany.
C MiethingDepartment of Hematology/Oncology, University Medical Center Freiburg, Freiburg, Germany.
J DuysterDepartment of Hematology/Oncology, University Medical Center Freiburg, Freiburg, Germany.
University Medical Center Freiburg · DEHelios Hospital Berlin-Buch · DEKlinikum rechts der Isar · DETechnical University of Munich · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The SH2-containing adaptor protein Grb10 was first identified in a yeast screen as a new binding partner for BCR-ABL and associates with BCR-ABL in a tyrosine-dependent manner. However, its function in BCR-ABL-mediated leukemogenesis in vivo is still unknown. Here we describe an important role of Grb10 in BCR-ABL-induced leukemia by using a versatile system for efficient oncogene expression and simultaneous Grb10 knockdown from a single vector. Primary bone marrow (BM) cells coexpressing Grb10-miR/BCR-ABL showed a significant decrease in colony formation and cell cycle progression. Transplantation of Grb10miR/BCR-ABL- or control-miR/BCR-ABL- transduced BM leads to a CML/B-ALL-like phenotype with significantly delayed disease onset and progression resulting in prolonged overall survival in Grb10-miR-transplanted mice. Methylcellulose experiments exhibit additive effects of imatinib treatment and Grb10 knockdown. Cell cycle analysis suggests an anti-proliferative effect of Grb10 knockdown in BCR-ABL(+) primary BM cells. However, Grb10 abrogation was not capable of completely abolishing the BCR-ABL-induced disease. Our findings were confirmed in the human BCR-ABL(+) cell line K562, where we demonstrate reduced viability, cell cycle progression and induction of apoptosis by stable Grb10 microRNA expression. Taken together, our results suggest that Grb10 knockdown in vivo leads to impaired proliferation, longer survival and reduced colony formation, suggesting an important role of Grb10 in BCR-ABL-mediated leukemogenesis.

Indexed as

Gene Expression Regulation, LeukemicAnimalsAntineoplastic AgentsApoptosisBenzamidesBone Marrow CellsCell CycleCell ProliferationDisease Models, AnimalFemaleFusion Proteins, bcr-ablGRB10 Adaptor ProteinHumansImatinib MesylateK562 CellsLeukemia, Myelogenous, Chronic, BCR-ABL Positiveabl-bcr fusion protein, humanAntineoplastic AgentsBenzamidesFusion Proteins, bcr-ablGRB10 Adaptor ProteinGrb10 protein, mouseImatinib MesylateMicroRNAsPiperazinesPyrimidinesRNA, Small Interfering

Identifiers

PMID25249015
OpenAlexW2006024446

What OpenQuestion holds

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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.