- AutorIn
- Friederike Pastore
- Alessandro Pastore
- Maja Rothenberg‐Thurley
- Klaus H. Metzeler
- Bianka Ksienzyk
- Stephanie Schneider
- Stefan K. Bohlander
- Jan Braess
- Maria C. Sauerland
- Dennis Görlich
- Wolfgang E. Berdel
- Bernhard Wörmann
- Michael S. von Bergwelt‐Baildon
- Wolfgang Hiddemann
- Karsten Spiekermann
- Titel
- Molecular profiling of patients with cytogenetically normal acute myeloid leukemia and hyperleukocytosis
- Zitierfähige Url:
- https://nbn-resolving.org/urn:nbn:de:bsz:15-qucosa2-979573
- Quellenangabe
- Cancer
Erscheinungsjahr: 2022
Seiten: 4215-4222
ISSN: 0008-543X
E-ISSN: 1097-0142 - Erstveröffentlichung
- 2022
- Abstract (EN)
- Acute myeloid leukemia (AML) with initial hyperleukocytosis is associated with high early mortality and a poor prognosis. The aims of this study were to delineate the underlying molecular landscape in the largest cytogenetic risk group, cytogenetically normal acute myeloid leukemia (CN‐AML), and to assess the prognostic relevance of recurrent mutations in the context of hyperleukocytosis and clinical risk factors. Methods: The authors performed a targeted sequencing of 49 recurrently mutated genes in 56 patients with newly diagnosed CN‐AML and initial hyperleukocytosis of ≥100 G/L treated in the AMLCG99 study. The median number of mutated genes per patient was 5. The most common mutations occurred in FLT3 (73%), NPM1 (75%), and TET2 (45%). Results: The predominant pathways affected by mutations were signaling (84% of patients), epigenetic modifiers (75% of patients), and nuclear transport (NPM1; 75%) of patients. AML with hyperleukocytosis was enriched for molecular subtypes that negatively affected the prognosis, including a high percentage of patients presenting
- Andere Ausgabe
- Link zur Erstveröffentlichung
DOI: 10.1002/cncr.34495 - Freie Schlagwörter (EN)
- acute myeloid leukemia (AML), hyperleukocytosis, molecular profiling, normal karyotype
- Klassifikation (DDC)
- 610
- Verlag
- Wiley-Liss, New York, NY
- Version / Begutachtungsstatus
- publizierte Version / Verlagsversion
- URN Qucosa
- urn:nbn:de:bsz:15-qucosa2-979573
- Veröffentlichungsdatum Qucosa
- 17.07.2025
- Dokumenttyp
- Artikel
- Sprache des Dokumentes
- Englisch
- Lizenz / Rechtehinweis
CC BY 4.0