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Mutations in myeloid transcription factors and activated signaling genes predict chronic myeloid leukemia outcomes

The result's identifiers

  • Result code in IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F65269705%3A_____%2F24%3A00079610" target="_blank" >RIV/65269705:_____/24:00079610 - isvavai.cz</a>

  • Alternative codes found

    RIV/00216224:14110/24:00135726

  • Result on the web

    <a href="https://ashpublications.org/bloodadvances/article/8/10/2361/515202/Mutations-in-myeloid-transcription-factors-and" target="_blank" >https://ashpublications.org/bloodadvances/article/8/10/2361/515202/Mutations-in-myeloid-transcription-factors-and</a>

  • DOI - Digital Object Identifier

    <a href="http://dx.doi.org/10.1182/bloodadvances.2023012127" target="_blank" >10.1182/bloodadvances.2023012127</a>

Alternative languages

  • Result language

    angličtina

  • Original language name

    Mutations in myeloid transcription factors and activated signaling genes predict chronic myeloid leukemia outcomes

  • Original language description

    Advancements in genomics are transforming the clinical management of chronic myeloid leukemia (CML) toward precision medicine. The impact of somatic mutations on treatment outcomes is still under debate. We studied the association of somatic mutations in epigenetic modifier genes and activated signaling/myeloid transcription factors (AS/MTFs) with disease progression and treatment failure in patients with CML after tyrosine kinase inhibitor (TKI) therapy. A total of 394 CML samples were sequenced, including 254 samples collected at initial diagnosis and 140 samples taken during follow-up. Single-molecule molecular inversion probe (smMIP)-based next-generation sequencing (NGS) was conducted targeting recurrently mutated loci in 40 genes, with a limit of detection of 0.2%. Seventy mutations were detected in 57 diagnostic samples (22.4%), whereas 64 mutations were detected in 39 of the follow-up samples (27.9%). Carrying any mutation at initial diagnosis was associated with worse outcomes after TKI therapy, particularly in AS/MTF genes. Patients having these mutations at initial diagnosis and treated with imatinib showed higher risks of treatment failure (hazard ratio, 2.53; 95% confidence interval, 1.13-5.66; P = .0239). The adverse prognostic impact of the mutations was not clear for patients treated with second-generation TKIs. The multivariate analysis affirmed that mutations in AS/MTF genes independently serve as adverse prognostic factors for molecular response, failure-free survival, and progression risk. Additionally, there was an observable nonsignificant trend indicating a heightened risk of progression to advanced disease and worse overall survival. In conclusion, mutations in the AS/MTF genes using smMIP-based NGS can help identify patients with a potential risk of both treatment failure and progression and may help upfront TKI selection. (C) 2024 by The American Society of Hematology.

  • Czech name

  • Czech description

Classification

  • Type

    J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database

  • CEP classification

  • OECD FORD branch

    30205 - Hematology

Result continuities

  • Project

  • Continuities

    N - Vyzkumna aktivita podporovana z neverejnych zdroju

Others

  • Publication year

    2024

  • Confidentiality

    S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Data specific for result type

  • Name of the periodical

    Blood Advances

  • ISSN

    2473-9529

  • e-ISSN

    2473-9537

  • Volume of the periodical

    8

  • Issue of the periodical within the volume

    10

  • Country of publishing house

    NL - THE KINGDOM OF THE NETHERLANDS

  • Number of pages

    12

  • Pages from-to

    2361-2372

  • UT code for WoS article

    001293872300001

  • EID of the result in the Scopus database

    2-s2.0-85195077302