Evidence map›Paper›PMID 24837466›Full record

Trial reportHaematologica2014

Distinct characteristics of e13a2 versus e14a2 BCR-ABL1 driven chronic myeloid leukemia under first-line therapy with imatinib.

Benjamin Hanfstein, Michael Lauseker, Rüdiger Hehlmann, Susanne Saussele, Philipp Erben, Christian Dietz, Alice Fabarius, Ulrike Proetel, Susanne Schnittger, Claudia Haferlach and 20 more

Abstract readRandomized Controlled Trial
In one paragraph

Trial report in Haematologica, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed, 2 pooled it
–field-weighted citation impact
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

59 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
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  14. High Level of CD8Cells · 2024
    Article
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  20. Effect ofTherapeutic advances in hematology · 2023
    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

30 authors.

Benjamin HanfsteinIII. Medizinische Klinik - Hämatologie und Onkologie, Universitätsmedizin Mannheim, Germany.
Michael LausekerInstitut für Medizinische Informationsverarbeitung, Biometrie und Epidemiologie der Ludwig-Maximilians-Universität München, Germany.
Rüdiger HehlmannIII. Medizinische Klinik - Hämatologie und Onkologie, Universitätsmedizin Mannheim, Germany.
Susanne SausseleIII. Medizinische Klinik - Hämatologie und Onkologie, Universitätsmedizin Mannheim, Germany.
Philipp ErbenIII. Medizinische Klinik - Hämatologie und Onkologie, Universitätsmedizin Mannheim, Germany.
Christian DietzIII. Medizinische Klinik - Hämatologie und Onkologie, Universitätsmedizin Mannheim, Germany.
Alice FabariusIII. Medizinische Klinik - Hämatologie und Onkologie, Universitätsmedizin Mannheim, Germany.
Ulrike ProetelIII. Medizinische Klinik - Hämatologie und Onkologie, Universitätsmedizin Mannheim, Germany.
Susanne SchnittgerMLL Münchner Leukämielabor, München, Germany.
Claudia HaferlachMLL Münchner Leukämielabor, München, Germany.
Stefan W KrauseMedizinische Klinik 5, Universitätsklinikum Erlangen, Germany.
Jörg SchubertKlinik für Hämatologie, Onkologie und Palliativmedizin, Evangelisches Krankenhaus Hamm, Germany.
Hermann EinseleMedizinische Klinik und Poliklinik II, Universitätsklinikum Würzburg, Germany.
Mathias HänelKlinik für Innere Medizin III, Klinikum Chemnitz, Germany.
Jolanta DenglerMedizinische Universitätsklinik, Abteilung Innere Medizin V, Ruprecht-Karls-Universität Heidelberg, Germany.
Christiane FalgeMedizinische Klinik 5, Klinikum Nürnberg Nord, Germany.
Lothar KanzMedizinische Klinik II, Universitätsklinikum Tübingen, Germany.
Andreas NeubauerKlinik für Innere Medizin, Schwerpunkt Hämatologie, Onkologie und Immunologie, Universitätsklinikum Gießen und Marburg, Marburg, Germany.
Michael KnebaII. Medizinische Klinik und Poliklinik im Städtischen Krankenhaus, Universitätsklinikum Schleswig-Holstein, Kiel, Germany.
Frank StegelmannKlinik für Innere Medizin III, Universitätsklinikum Ulm, Germany.
Michael PfreundschuhInnere Medizin I, Universitätsklinikum des Saarlandes, Homburg/Saar, Germany.
Cornelius F WallerKlinik für Innere Medizin I, Universitätsklinikum Freiburg, Germany.
Karsten SpiekermannMedizinische Klinik und Poliklinik III, Ludwig-Maximilians-Universität München, Germany.
Gabriela M BaerlocherUniversitätsklinik für Hämatologie, Inselspital Bern, Switzerland.
Markus PfirrmannInstitut für Medizinische Informationsverarbeitung, Biometrie und Epidemiologie der Ludwig-Maximilians-Universität München, Germany.
Joerg HasfordInstitut für Medizinische Informationsverarbeitung, Biometrie und Epidemiologie der Ludwig-Maximilians-Universität München, Germany.
Wolf-Karsten HofmannIII. Medizinische Klinik - Hämatologie und Onkologie, Universitätsmedizin Mannheim, Germany.
Andreas HochhausAbteilung für Hämatologie und Onkologie, Klinik für Innere Medizin II, Universitätsklinikum Jena, Germany.
Martin C MüllerIII. Medizinische Klinik - Hämatologie und Onkologie, Universitätsmedizin Mannheim, Germany martin.mueller@medma.uni-heidelberg.de.
SAKK and the German CML Study Group

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The vast majority of chronic myeloid leukemia patients express a BCR-ABL1 fusion gene mRNA encoding a 210 kDa tyrosine kinase which promotes leukemic transformation. A possible differential impact of the corresponding BCR-ABL1 transcript variants e13a2 ("b2a2") and e14a2 ("b3a2") on disease phenotype and outcome is still a subject of debate. A total of 1105 newly diagnosed imatinib-treated patients were analyzed according to transcript type at diagnosis (e13a2, n=451; e14a2, n=496; e13a2+e14a2, n=158). No differences regarding age, sex, or Euro risk score were observed. A significant difference was found between e13a2 and e14a2 when comparing white blood cells (88 vs. 65 × 10(9)/L, respectively; P<0.001) and platelets (296 vs. 430 × 10(9)/L, respectively; P<0.001) at diagnosis, indicating a distinct disease phenotype. No significant difference was observed regarding other hematologic features, including spleen size and hematologic adverse events, during imatinib-based therapies. Cumulative molecular response was inferior in e13a2 patients (P=0.002 for major molecular response; P<0.001 for MR4). No difference was observed with regard to cytogenetic response and overall survival. In conclusion, e13a2 and e14a2 chronic myeloid leukemia seem to represent distinct biological entities. However, clinical outcome under imatinib treatment was comparable and no risk prediction can be made according to e13a2 versus e14a2 BCR-ABL1 transcript type at diagnosis. (clinicaltrials.gov identifier:00055874).

Indexed as

AdolescentAdultAgedAged, 80 and overAlternative SplicingAntineoplastic AgentsBenzamidesBlood PlateletsDrug MonitoringFemaleFusion Proteins, bcr-ablGenotypeHumansImatinib MesylateLeukemia, Myelogenous, Chronic, BCR-ABL PositiveLeukocytesAntineoplastic AgentsBCR-ABL1 fusion protein, humanBenzamidesFusion Proteins, bcr-ablImatinib MesylatePiperazinesPyrimidinesRNA, Messenger

Identifiers

PMID24837466
PMCPMC4562532

What OpenQuestion holds

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Read underepoch 390

Registered trials

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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.