Evidence map›Paper›PMID 35902731›Full record

ArticleLeukemia2022

ASXL1 mutations predict inferior molecular response to nilotinib treatment in chronic myeloid leukemia.

Lioba Schönfeld, Jenny Rinke, Anna Hinze, Saskia N Nagel, Vivien Schäfer, Thomas Schenk, Christian Fabisch, Tim H Brümmendorf, Andreas Burchert, Philipp le Coutre and 6 more

Open access · hybridAbstract read
In one paragraph

Article in Leukemia, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 2 pooled it
8.0field-weighted citation impact, top 2% 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

42 citing papers in PubMed, 2 syntheses or guidelines pooled it, 52 citations in OpenAlex.

  1. [Guideline for the diagnosis and treatment of chronic myeloid leukemia in China (2025)].Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi · 2025
    Guideline
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  17. EarlyCancers · 2025
    Article
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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

16 authors at 6 institutions in 2 countries.

Lioba Schönfeld *Abteilung Hämatologie und Internistische Onkologie, Klinik für Innere Medizin II, Universitätsklinikum Jena, Jena, Germany.
Jenny Rinke *Abteilung Hämatologie und Internistische Onkologie, Klinik für Innere Medizin II, Universitätsklinikum Jena, Jena, Germany.
Anna HinzeAbteilung Hämatologie und Internistische Onkologie, Klinik für Innere Medizin II, Universitätsklinikum Jena, Jena, Germany.
Saskia N NagelAbteilung Hämatologie und Internistische Onkologie, Klinik für Innere Medizin II, Universitätsklinikum Jena, Jena, Germany.
Vivien SchäferAbteilung Hämatologie und Internistische Onkologie, Klinik für Innere Medizin II, Universitätsklinikum Jena, Jena, Germany.
Thomas SchenkAbteilung Hämatologie und Internistische Onkologie, Klinik für Innere Medizin II, Universitätsklinikum Jena, Jena, Germany.
Christian FabischAbteilung Hämatologie und Internistische Onkologie, Klinik für Innere Medizin II, Universitätsklinikum Jena, Jena, Germany.
Tim H BrümmendorfDepartment of Hematology, Oncology, Hemostaseology and Stem Cell Transplantation, Medical Faculty, RWTH Aachen University, Aachen, Germany.ORCID http://orcid.org/0000-0002-9677-3723
Andreas BurchertKlinik für Innere Medizin, Schwerpunkt Hämatologie, Onkologie und Immunologie, Universitätsklinikum Marburg, Marburg, Germany.ORCID http://orcid.org/0000-0002-8411-8844
Philipp le CoutreMedizinische Klinik, Hämatologie und Onkologie, Charité - Universitätsmedizin Berlin, Berlin, Germany.
Stefan W KrauseMedizinische Klinik 5 (Hämatologie und Internistische Onkologie), Universitätsklinikum Erlangen, Erlangen, Germany.ORCID http://orcid.org/0000-0002-5259-4651
Susanne SausseleIII. Medizinische Klinik, Medizinische Fakultät Mannheim der Universität Heidelberg, Mannheim, Germany.ORCID http://orcid.org/0000-0003-0357-5785
Fatemeh SafizadehInstitut für Medizinische Informationsverarbeitung, Biometrie und Epidemiologie - IBE, Ludwig-Maximilians-Universität, München, Germany.
Markus PfirrmannInstitut für Medizinische Informationsverarbeitung, Biometrie und Epidemiologie - IBE, Ludwig-Maximilians-Universität, München, Germany.ORCID http://orcid.org/0000-0002-8948-0690
Andreas HochhausAbteilung Hämatologie und Internistische Onkologie, Klinik für Innere Medizin II, Universitätsklinikum Jena, Jena, Germany.ORCID http://orcid.org/0000-0003-0626-0834
Thomas ErnstAbteilung Hämatologie und Internistische Onkologie, Klinik für Innere Medizin II, Universitätsklinikum Jena, Jena, Germany. thomas.ernst@med.uni-jena.de.ORCID http://orcid.org/0000-0003-2147-489X
Jena University Hospital · DEZimmer Biomet (Netherlands) · NLCharité - Universitätsmedizin Berlin · DEHeidelberg University · DERWTH Aachen University · DEUniversitätsklinikum Erlangen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gene mutations independent of BCR::ABL1 have been identified in newly diagnosed patients with chronic myeloid leukemia (CML) in chronic phase, whereby mutations in epigenetic modifier genes were most common. These findings prompted the systematic analysis of prevalence, dynamics, and prognostic significance of such mutations, in a clinically well-characterized patient population of 222 CML patients from the TIGER study (CML-V) by targeted next-generation sequencing covering 54 myeloid leukemia-associated genes. In total, 53/222 CML patients (24%) carried 60 mutations at diagnosis with ASXL1 being most commonly affected (n = 20). To study mutation dynamics, longitudinal deep sequencing analysis of serial samples was performed in 100 patients after 12, 24, and 36 months of therapy. Typical patterns of clonal evolution included eradication, persistence, and emergence of mutated clones. Patients carrying an ASXL1 mutation at diagnosis showed a less favorable molecular response to nilotinib treatment, as a major molecular response (MMR) was achieved less frequently at month 12, 18, and 24 compared to all other patients. Patients with ASXL1 mutations were also younger and more frequently found in the high risk category, suggesting a central role of clonal evolution associated with ASXL1 mutations in CML pathogenesis.

Indexed as

Fusion Proteins, bcr-ablLeukemia, Myelogenous, Chronic, BCR-ABL PositiveHumansMutationProtein Kinase InhibitorsPyrimidinesRepressor ProteinsASXL1 protein, humanFusion Proteins, bcr-ablnilotinibProtein Kinase InhibitorsPyrimidinesRepressor Proteins

Identifiers

PMID35902731
PMCPMC9417980
OpenAlexW4288077415

What OpenQuestion holds

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LicenceCC BY
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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.