Evidence map›Paper›PMID 37161070›Full record

ArticleLeukemia2023

Mast cell deficiency prevents BCR::ABL1 induced splenomegaly and cytokine elevation in a CML mouse model.

Melanie Langhammer, Julia Schöpf, Timo Jaquet, Katharina Horn, Moritz Angel, Corinna Spohr, Daniel Christen, Franziska Maria Uhl, Tiago Maié, Henrike Jacobi and 15 more

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Leukemia, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
0.6field-weighted citation impact, top 29% 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

0 citing papers in PubMed, 2 citations in OpenAlex.

No citing paper in PubMed yet.

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

25 authors at 3 institutions in 1 country.

Melanie Langhammer *Institute of Molecular Medicine, ZBMZ, Faculty of Medicine, University of Freiburg, Freiburg, Germany.ORCID http://orcid.org/0009-0008-7743-2879
Julia Schöpf *Institute of Molecular Medicine, ZBMZ, Faculty of Medicine, University of Freiburg, Freiburg, Germany.
Timo JaquetDepartment of Hematology, Oncology, Hemostaseology, and Stem Cell Transplantation, Faculty of Medicine, RWTH Aachen University, Aachen, Germany.
Katharina HornInstitute of Biochemistry and Molecular Immunology, RWTH Aachen University, Aachen, Germany.
Moritz AngelInstitute of Molecular Medicine, ZBMZ, Faculty of Medicine, University of Freiburg, Freiburg, Germany.ORCID http://orcid.org/0009-0003-5644-0515
Corinna SpohrInstitute of Molecular Medicine, ZBMZ, Faculty of Medicine, University of Freiburg, Freiburg, Germany.
Daniel ChristenInstitute of Molecular Medicine, ZBMZ, Faculty of Medicine, University of Freiburg, Freiburg, Germany.
Franziska Maria UhlFaculty of Biology, University of Freiburg, Freiburg, Germany.ORCID http://orcid.org/0000-0001-8951-6289
Tiago MaiéInstitute for Computational Genomics, University Hospital, RWTH Aachen University, Aachen, Germany.ORCID http://orcid.org/0000-0003-4857-4014
Henrike JacobiDepartment of Hematology, Oncology, Hemostaseology, and Stem Cell Transplantation, Faculty of Medicine, RWTH Aachen University, Aachen, Germany.
Thorsten B FeyerabendDivision of Cellular Immunology, German Cancer Research Center (DKFZ), Heidelberg, Germany.
Julia HuberDepartment of Pathology, Institute for Surgical Pathology, Medical Center, Faculty of Medicine, University of Freiburg, Freiburg, Germany.
Marcus PanningInstitute of Virology, Medical Center, Faculty of Medicine, University of Freiburg, Freiburg, Germany.
Cassian SitaruDepartment of Dermatology, Medical Center, Faculty of Medicine, University of Freiburg, Freiburg, Germany.
Ivan CostaInstitute for Computational Genomics, University Hospital, RWTH Aachen University, Aachen, Germany.ORCID http://orcid.org/0000-0003-2890-8697
Robert ZeiserDepartment of Medicine I, Medical Center, Faculty of Medicine, University of Freiburg, Freiburg, Germany.ORCID http://orcid.org/0000-0001-6565-3393
Konrad AumannDepartment of Pathology, Institute for Surgical Pathology, Medical Center, Faculty of Medicine, University of Freiburg, Freiburg, Germany.
Heiko BeckerDepartment of Medicine I, Medical Center, Faculty of Medicine, University of Freiburg, Freiburg, Germany.
Till BraunschweigDepartment of Pathology, University Hospital, RWTH Aachen University, Aachen, Germany.
Steffen KoschmiederDepartment of Hematology, Oncology, Hemostaseology, and Stem Cell Transplantation, Faculty of Medicine, RWTH Aachen University, Aachen, Germany.ORCID http://orcid.org/0000-0002-1011-8171
Khalid ShoumariyehDepartment of Medicine I, Medical Center, Faculty of Medicine, University of Freiburg, Freiburg, Germany.
Michael HuberInstitute of Biochemistry and Molecular Immunology, RWTH Aachen University, Aachen, Germany.ORCID http://orcid.org/0000-0001-7222-8686
Mirle Schemionek-ReindersDepartment of Hematology, Oncology, Hemostaseology, and Stem Cell Transplantation, Faculty of Medicine, RWTH Aachen University, Aachen, Germany.ORCID http://orcid.org/0000-0002-5947-3529
Tilman BrummerInstitute of Molecular Medicine, ZBMZ, Faculty of Medicine, University of Freiburg, Freiburg, Germany.ORCID http://orcid.org/0000-0003-4387-7905
Sebastian HalbachInstitute of Molecular Medicine, ZBMZ, Faculty of Medicine, University of Freiburg, Freiburg, Germany. Sebastian.Halbach@mol-med.uni-freiburg.de.ORCID http://orcid.org/0000-0002-6827-8178
University of Freiburg · DERWTH Aachen University · DEGerman Cancer Research Center · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The persistence of leukemic stem cells (LSCs) represents a problem in the therapy of chronic myeloid leukemia (CML). Hence, it is of utmost importance to explore the underlying mechanisms to develop new therapeutic approaches to cure CML. Using the genetically engineered ScltTA/TRE-BCR::ABL1 mouse model for chronic phase CML, we previously demonstrated that the loss of the docking protein GAB2 counteracts the infiltration of mast cells (MCs) in the bone marrow (BM) of BCR::ABL1 positive mice. Here, we show for the first time that BCR::ABL1 drives the cytokine independent expansion of BM derived MCs and sensitizes them for FcεRI triggered degranulation. Importantly, we demonstrate that genetic mast cell deficiency conferred by the Cpa3

Indexed as

Leukemia, Myelogenous, Chronic, BCR-ABL PositiveLeukemia, MyeloidAnimalsCytokinesDisease Models, AnimalFusion Proteins, bcr-ablHumansMast CellsMiceProtein Kinase InhibitorsSplenomegalyTumor MicroenvironmentCytokinesFusion Proteins, bcr-ablProtein Kinase Inhibitors

Identifiers

PMID37161070
PMCPMC10317838
OpenAlexW4376121319

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.