Monosomal karyotype and chromosome 17p loss or TP53 mutations in decitabine-treated patients with acute myeloid leukemia View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2020-06-06

AUTHORS

Heiko Becker, Dietmar Pfeifer, Gabriele Ihorst, Milena Pantic, Julius Wehrle, Björn H. Rüter, Lars Bullinger, Björn Hackanson, Ulrich Germing, Andrea Kuendgen, Uwe Platzbecker, Konstanze Döhner, Arnold Ganser, Anne Hagemeijer, Pierre W. Wijermans, Hartmut Döhner, Justus Duyster, Michael Lübbert

ABSTRACT

TP53 aberrations reportedly predict favorable responses to decitabine (DAC) in acute myeloid leukemia (AML). We evaluated clinical features and outcomes associated with chromosome 17p loss or TP53 gene mutations in older, unfit DAC-treated AML patients in a phase II trial. Of 178 patients, 25 had loss of 17p in metaphase cytogenetics; 24 of these had a complex (CK+) and 21 a monosomal karyotype (MK+). In analyses in all patients and restricted to CK+ and MK+ patients, 17p loss tended to associate with higher rates of complete remission (CR), partial remission (PR), or antileukemic effect (ALE). Despite favorable response rates, there was no significant OS difference between patients with or without loss of 17p in the entire cohort or in the CK+ and MK+ cohort. TP53 mutations were identified in eight of 45 patients with material available. Five of the eight TP53-mutated patients had 17p loss. TP53-mutated patients had similar rates of CR/PR/ALE but shorter OS than those with TP53 wild type (P = 0.036). Moreover, patients with a subclone based on mutation data had shorter OS than those without (P = 0.05); only one patient with TP53-mutated AML had a subclone. In conclusion, 17p loss conferred a favorable impact on response rates, even among CK+ and MK+ patients that however could not be maintained. The effect of TP53 mutations appeared to be different; however, patient numbers were low. Future research needs to further dissect the impact of the various TP53 aberrations in HMA-based combination therapies. The limited duration of favorable responses to HMA treatment in adverse-risk genetics AML should prompt physicians to advance allografting for eligible patients in a timely fashion. More... »

PAGES

1551-1560

References to SciGraph publications

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  • Journal

    TITLE

    Annals of Hematology

    ISSUE

    7

    VOLUME

    99

    Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1007/s00277-020-04082-7

    DOI

    http://dx.doi.org/10.1007/s00277-020-04082-7

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1128250197

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/32504186


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