Evidence map›Paper›PMID 26686248›Full record

ArticleLeukemia2016

The target cell of transformation is distinct from the leukemia stem cell in murine CALM/AF10 leukemia models.

S Dutta, A Krause, S Vosberg, T Herold, B Ksienzyk, L Quintanilla-Martinez, B Tizazu, M Chopra, A Graf, S Krebs and 11 more

Abstract read
PubMed Publisher
In one paragraph

Article in Leukemia, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.8field-weighted citation impact, top 24% 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

9 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
  2. EJHaem · 2024
    Article
  3. Article
  4. Article
  5. Article
  6. CCAAT/enhancer-binding protein alpha (CEBPA) gene haploinsufficiency does not alter hematopoiesis or induce leukemia in Lck-CALM/AF10 transgenic mice.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2019
    Article
  7. Blood advances · 2018
    Article
  8. Review
  9. 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

21 authors at 6 institutions in 3 countries.

S DuttaDepartment of Medicine III, University Hospital Grosshadern, Ludwig Maximilians-University, Munich, Germany.
A KrauseDepartment of Small Animal Medicine, Federal University of Santa Maria, Santa Maria, Rio Grande do Sul, Brazil.
S VosbergDepartment of Medicine III, University Hospital Grosshadern, Ludwig Maximilians-University, Munich, Germany.
T HeroldDepartment of Medicine III, University Hospital Grosshadern, Ludwig Maximilians-University, Munich, Germany.
B KsienzykDepartment of Medicine III, University Hospital Grosshadern, Ludwig Maximilians-University, Munich, Germany.
L Quintanilla-MartinezInstitute for Pathology, University Hospital and Faculty of Medicine, University of Tübingen, Tübingen, Germany.
B TizazuDepartment of Medicine III, University Hospital Grosshadern, Ludwig Maximilians-University, Munich, Germany.
M ChopraDepartment of Molecular Medicine and Pathology, Faculty of Medical and Health Sciences, The University of Auckland, Auckland, New Zealand.
A GrafLaboratory for Functional Genome Analysis, Gene Center, Ludwig Maximilians-University, Munich, Germany.
S KrebsLaboratory for Functional Genome Analysis, Gene Center, Ludwig Maximilians-University, Munich, Germany.
H BlumLaboratory for Functional Genome Analysis, Gene Center, Ludwig Maximilians-University, Munich, Germany.
P A GreifDepartment of Medicine III, University Hospital Grosshadern, Ludwig Maximilians-University, Munich, Germany.
A VetterDepartment of Medicine III, University Hospital Grosshadern, Ludwig Maximilians-University, Munich, Germany.
K MetzelerDepartment of Medicine III, University Hospital Grosshadern, Ludwig Maximilians-University, Munich, Germany.
M Rothenberg-ThurleyDepartment of Medicine III, University Hospital Grosshadern, Ludwig Maximilians-University, Munich, Germany.
M R SchneiderInstitute of Molecular Animal Breeding and Biotechnology, Ludwig Maximilians-University, Munich, Germany.
M DahlhoffInstitute of Molecular Animal Breeding and Biotechnology, Ludwig Maximilians-University, Munich, Germany.
K SpiekermannDepartment of Medicine III, University Hospital Grosshadern, Ludwig Maximilians-University, Munich, Germany.
U Zimber-StroblDepartment of Gene Vectors, Helmholtz Zentrum München, German Research Center for Environmental Health, Munich, Germany.
E WolfInstitute of Molecular Animal Breeding and Biotechnology, Ludwig Maximilians-University, Munich, Germany.
S K BohlanderDepartment of Molecular Medicine and Pathology, Faculty of Medical and Health Sciences, The University of Auckland, Auckland, New Zealand.
Ludwig-Maximilians-Universität München · DEHelmholtz Zentrum München · DEDeutschen Konsortium für Translationale Krebsforschung · DEUniversity of Auckland · NZUniversidade Federal de Santa Maria · BRUniversity of Tübingen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The CALM/AF10 fusion gene is found in various hematological malignancies including acute myeloid leukemia (AML), T-cell acute lymphoblastic leukemia and malignant lymphoma. We have previously identified the leukemia stem cell (LSC) in a CALM/AF10-driven murine bone marrow transplant AML model as B220+ lymphoid cells with B-cell characteristics. To identify the target cell for leukemic transformation or 'cell of origin of leukemia' (COL) in non-disturbed steady-state hematopoiesis, we inserted the CALM/AF10 fusion gene preceded by a loxP-flanked transcriptional stop cassette into the Rosa26 locus. Vav-Cre-induced panhematopoietic expression of the CALM/AF10 fusion gene led to acute leukemia with a median latency of 12 months. Mice expressing CALM/AF10 in the B-lymphoid compartment using Mb1-Cre or CD19-Cre inducer lines did not develop leukemia. Leukemias had a predominantly myeloid phenotype but showed coexpression of the B-cell marker B220, and had clonal B-cell receptor rearrangements. Using whole-exome sequencing, we identified an average of two to three additional mutations per leukemia, including activating mutations in known oncogenes such as FLT3 and PTPN11. Our results show that the COL for CALM/AF10 leukemia is a stem or early progenitor cell and not a cell of B-cell lineage with a phenotype similar to that of the LSC in CALM/AF10+ leukemia.

Indexed as

AnimalsB-LymphocytesCell Transformation, NeoplasticExomeGenetic EngineeringLeukemia, ExperimentalMiceMutationNeoplastic Stem CellsOncogene Proteins, FusionSequence Analysis, DNAAF10-CALM fusion protein, humanOncogene Proteins, Fusion

Identifiers

PMID26686248
OpenAlexW2215459348

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.