Evidence map›Paper›PMID 24603533›Full record

ArticleLeukemia2014

A 'telomere-associated secretory phenotype' cooperates with BCR-ABL to drive malignant proliferation of leukemic cells.

M Braig, N Pällmann, M Preukschas, D Steinemann, W Hofmann, A Gompf, T Streichert, T Braunschweig, M Copland, K L Rudolph and 5 more

Abstract read
PubMed Publisher
In one paragraph

Article in Leukemia, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

33 citing papers in PubMed, 37 citations in OpenAlex.

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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

15 authors at 9 institutions in 3 countries.

M Braig1] Department of Oncology/Hematology and Bone Marrow Transplantation with Section of Pneumology, Hubertus Wald Tumor-Zentrum, University Hospital Hamburg-Eppendorf, Hamburg, Germany [2] Division of Hematology, University Hospital Zürich, Zürich, Switzerland.
N PällmannDepartment of Oncology/Hematology and Bone Marrow Transplantation with Section of Pneumology, Hubertus Wald Tumor-Zentrum, University Hospital Hamburg-Eppendorf, Hamburg, Germany.
M PreukschasDepartment of Oncology/Hematology and Bone Marrow Transplantation with Section of Pneumology, Hubertus Wald Tumor-Zentrum, University Hospital Hamburg-Eppendorf, Hamburg, Germany.
D SteinemannInstitute of Cell and Molecular Pathology, Hannover Medical School, Hannover, Germany.
W HofmannInstitute of Cell and Molecular Pathology, Hannover Medical School, Hannover, Germany.
A GompfInstitute of Molecular Medicine and Max-Planck-Research Group on Stem Cell Aging, Ulm, Germany.
T StreichertInstitute of Clinical Chemistry, University Hospital Cologne, Cologne, Germany.
T BraunschweigDepartment of Pathology, University Hospital of the RWTH Aachen, Aachen, Germany.
M CoplandPaul O'Gorman Leukaemia Research Centre, College of Medical, Veterinary and Life Sciences, Institute of Cancer Sciences, University of Glasgow, Scotland, UK.
K L RudolphLeibniz Institute of Age Research - Fritz-Lipmann Institute (FLI), Jena, Germany.
C BokemeyerDepartment of Oncology/Hematology and Bone Marrow Transplantation with Section of Pneumology, Hubertus Wald Tumor-Zentrum, University Hospital Hamburg-Eppendorf, Hamburg, Germany.
S KoschmiederDepartment of Hematology and Oncology, University Hospital of the RWTH Aachen, Aachen, Germany.
A SchuppertAachen Institute for Advanced Study in Computational Engineering Science (AICES), RWTH Aachen University, Aachen, Germany.
S Balabanov1] Department of Oncology/Hematology and Bone Marrow Transplantation with Section of Pneumology, Hubertus Wald Tumor-Zentrum, University Hospital Hamburg-Eppendorf, Hamburg, Germany [2] Division of Hematology, University Hospital Zürich, Zürich, Switzerland.
T H BrümmendorfDepartment of Hematology and Oncology, University Hospital of the RWTH Aachen, Aachen, Germany.
RWTH Aachen University · DEUniversity Cancer Center Hamburg · DEMedizinische Hochschule Hannover · DELeibniz Institute on Aging - Fritz Lipmann Institute (FLI) · DEUniversität Ulm · DEUniversity Hospital Cologne · DEUniversity Hospital of Zurich · CHUniversity Medical Center Hamburg-Eppendorf · DEUniversity of Glasgow · GB

Funding

Chief Scientist Office SCD/04
6 · The paper itself

Abstract

Telomere biology is frequently associated with disease evolution in human cancer and dysfunctional telomeres have been demonstrated to contribute to genetic instability. In BCR-ABL(+) chronic myeloid leukemia (CML), accelerated telomere shortening has been shown to correlate with leukemia progression, risk score and response to treatment. Here, we demonstrate that proliferation of murine CML-like bone marrow cells strongly depends on telomere maintenance. CML-like cells of telomerase knockout mice with critically short telomeres (CML-iG4) are growth retarded and proliferation is terminally stalled by a robust senescent cell cycle arrest. In sharp contrast, CML-like cells with pre-shortened, but not critically short telomere lengths (CML-G2) grew most rapidly and were found to express a specific 'telomere-associated secretory phenotype', comprising secretion of chemokines, interleukins and other growth factors, thereby potentiating oncogene-driven growth. Moreover, conditioned supernatant of CML-G2 cells markedly enhanced proliferation of CML-WT and pre-senescent CML-iG4 cells. Strikingly, a similar inflammatory mRNA expression pattern was found with disease progression from chronic phase to accelerated phase in CML patients. These findings demonstrate that telomere-induced senescence needs to be bypassed by leukemic cells in order to progress to blast crisis and provide a novel mechanism by which telomere shortening may contribute to disease evolution in CML.

Indexed as

Cell ProliferationGene Expression Regulation, LeukemicAnimalsApoptosisBone Marrow CellsCell CycleCell Line, TumorCellular SenescenceChemokinesCytokinesDisease ProgressionFusion Proteins, bcr-ablHumansInflammationLeukemiaMiceChemokinesCytokinesFusion Proteins, bcr-abl

Identifiers

PMID24603533
OpenAlexW2018892615

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.