Outcomes of acute myeloid leukemia with myelodysplasia related changes depend on diagnostic criteria and therapy.


Journal

American journal of hematology
ISSN: 1096-8652
Titre abrégé: Am J Hematol
Pays: United States
ID NLM: 7610369

Informations de publication

Date de publication:
06 2020
Historique:
received: 03 01 2020
revised: 20 02 2020
accepted: 27 02 2020
pubmed: 1 3 2020
medline: 24 6 2020
entrez: 1 3 2020
Statut: ppublish

Résumé

Acute myeloid leukemia with myelodysplasia-related changes (AML-MRC) is a heterogeneous disorder defined by multilineage dysplasia, myelodysplastic syndrome (MDS)-related karyotype, or history of prior MDS. We evaluated 415 patients with AML-MRC treated from 2013 to 2018 and analyzed their clinical outcomes based on the diagnostic criteria of AML-MRC, therapy type and mutation profile. Criteria for AML-MRC included: cytogenetic abnormalities (AML-MRC-C) in 243 (59%), prior history of MDS in 75 (18%) including 47 (11%) with previously untreated MDS (AML-MRC-H) and 28 (7%) with previously treated MDS (AML-MRC-TS), and 97 (23%) with multilineage dysplasia (AML-MRC-M). Median age was 70 years (range 18-94). Among 95 evaluable patients, a total of 37 (39%) had secondary-type (ASXL1, BCOR, EZH2, SF3B1, SRSF2, STAG2, U2AF1, ZRSR2) mutations. Mutations in ASXL1, BCOR, SF3B1, SRSF2, and U2AF1 tended to appear in dominant clones. By multivariate analysis, AML-MRC subtype, age and serum LDH levels were independent predictors of outcome, with patients with AML-MRC-M (HR 0.56, CI 0.38-0.84, P = .004) and AML-MRC-H having better OS. Compared to a cohort of 468 patients with AML without MRC, patients with AML-MRC-M/AML-MRC-H had similar outcomes to those with intermediate risk AML by European LeukemiaNet criteria. Intensive therapy was associated with improved OS in patients with AML-MRC-M (HR 0.42, CI 0.19-0.94, P = .036) and with improved EFS in AML-MRC-M and AML-MRC-H (HR 0.26, CI 0.10-0.63, P = .003). This data suggests that not all diagnostic criteria for AML-MRC define high-risk patients and that specific subgroups may benefit from different therapeutic interventions.

Identifiants

pubmed: 32112433
doi: 10.1002/ajh.25769
doi:

Substances chimiques

Bridged Bicyclo Compounds, Heterocyclic 0
CPX-351 0
Neoplasm Proteins 0
Sulfonamides 0
Cytarabine 04079A1RDZ
venetoclax N54AIC43PW
Daunorubicin ZS7284E0ZP

Types de publication

Clinical Trial Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

612-622

Informations de copyright

© 2020 Wiley Periodicals, Inc.

Références

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Auteurs

Guillermo Montalban-Bravo (G)

Department of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.

Rashmi Kanagal-Shamanna (R)

Department of Hematopathology, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.

Caleb A Class (CA)

Department of Biostatistics, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.

Koji Sasaki (K)

Department of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.

Farhad Ravandi (F)

Department of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.

Jorge E Cortes (JE)

Department of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.

Naval Daver (N)

Department of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.

Koichi Takahashi (K)

Department of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.

Nicholas J Short (NJ)

Department of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.

Courtney D DiNardo (CD)

Department of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.

Elias Jabbour (E)

Department of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.

Gautam Borthakur (G)

Department of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.

Kiran Naqvi (K)

Department of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.

Ghayas C Issa (GC)

Department of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.

Marina Konopleva (M)

Department of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.

Joseph D Khoury (JD)

Department of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.

Mark Routbort (M)

Department of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.

Sherry Pierce (S)

Department of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.

Kim-Anh Do (KA)

Department of Biostatistics, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.

Carlos Bueso-Ramos (C)

Department of Hematopathology, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.

Keyur Patel (K)

Department of Hematopathology, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.

Hagop Kantarjian (H)

Department of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.

Guillermo Garcia-Manero (G)

Department of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.

Tapan M Kadia (TM)

Department of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.

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