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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.

Titel:	Monosomal karyotype and chromosome 17p loss or TP53 mutations in decitabine-treated patients with acute myeloid leukemia.
Autor/in / Beteiligte Person:	Becker, H ; Pfeifer, D ; Ihorst, G ; Pantic, M ; Wehrle, J ; Rüter, BH ; Bullinger, L ; Hackanson, B ; Germing, U ; Kuendgen, A ; Platzbecker, U ; Döhner, K ; Ganser, A ; Hagemeijer, A ; Wijermans, PW ; Döhner, H ; Duyster, J ; Lübbert, M
Link:	Full Text Finder (Volltext)
Zeitschrift:	Annals of hematology, Jg. 99 (2020-07-01), Heft 7, S. 1551-1560
Veröffentlichung:	Berlin : Springer Verlag ; <i>Original Publication</i>: Berlin ; New York : Springer International, c1991-, 2020
Medientyp:	academicJournal
ISSN:	1432-0584 (electronic)
DOI:	10.1007/s00277-020-04082-7
Schlagwort:	Aged Aged, 80 and over Chromosomes, Human, Pair 17 genetics Clonal Evolution drug effects Clonal Evolution genetics DNA Mutational Analysis Female Germany epidemiology Humans Karyotype Karyotyping Leukemia, Myeloid, Acute epidemiology Leukemia, Myeloid, Acute pathology Male Middle Aged Mutation Survival Analysis Chromosome Deletion Decitabine therapeutic use Leukemia, Myeloid, Acute drug therapy Leukemia, Myeloid, Acute genetics Monosomy diagnosis Monosomy genetics Smith-Magenis Syndrome diagnosis Smith-Magenis Syndrome epidemiology Smith-Magenis Syndrome genetics Tumor Suppressor Protein p53 genetics
Sonstiges:	Nachgewiesen in: MEDLINE Sprachen: English Publication Type: Clinical Trial, Phase II; Journal Article Language: English [Ann Hematol] 2020 Jul; Vol. 99 (7), pp. 1551-1560. <i>Date of Electronic Publication: </i>2020 Jun 06. MeSH Terms: Chromosome Deletion* ; Monosomy* / diagnosis ; Monosomy* / genetics ; Smith-Magenis Syndrome* / diagnosis ; Smith-Magenis Syndrome* / epidemiology ; Smith-Magenis Syndrome* / genetics ; Decitabine / therapeutic use ; Leukemia, Myeloid, Acute / drug therapy ; Leukemia, Myeloid, Acute / genetics ; Tumor Suppressor Protein p53 / genetics ; Aged ; Aged, 80 and over ; Chromosomes, Human, Pair 17 / genetics ; Clonal Evolution / drug effects ; Clonal Evolution / genetics ; DNA Mutational Analysis ; Female ; Germany / epidemiology ; Humans ; Karyotype ; Karyotyping ; Leukemia, Myeloid, Acute / epidemiology ; Leukemia, Myeloid, Acute / pathology ; Male ; Middle Aged ; Mutation ; Survival Analysis References: Jung HA, Maeng CH, Kim M, Kim S, Jung CW, Jang JH (2015) Platelet response during the second cycle of decitabine treatment predicts response and survival for myelodysplastic syndrome patients. 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J Clin Oncol 38:257–270. https://doi.org/10.1200/JCO.19.01053. (PMID: 10.1200/JCO.19.0105331794324) Grant Information: SPP 1463 ML 429/8-1; CRC 992 MEDEP C04; FOR 2674 LU 429/16-1 Deutsche Forschungsgemeinschaft; FOR 2674 BE 6461/1-1 Deutsche Forschungsgemeinschaft; 111210 Deutsche Krebshilfe; Exploration Grant Boehringer Ingelheim Stiftung Contributed Indexing: Keywords: AML; Acute myeloid leukemia; Decitabine; Monosomy; Mutations; TP53 Substance Nomenclature: 0 (TP53 protein, human) ; 0 (Tumor Suppressor Protein p53) ; 776B62CQ27 (Decitabine) SCR Disease Name: Chromosome 17 deletion Entry Date(s): Date Created: 20200607 Date Completed: 20200723 Latest Revision: 20211007 Update Code: 20231215 PubMed Central ID: PMC7316846

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