TP53 mutation status divides myelodysplastic syndromes with complex karyotypes into distinct prognostic subgroups

Detlef Haase(University of Göttingen), Kristen E. Stevenson(Dana-Farber Cancer Institute), Donna Neuberg(Dana-Farber Cancer Institute), Jaroslaw P. Maciejewski(Cleveland Clinic), Aziz Nazha(Cleveland Clinic), Mikkael A. Sekeres(Cleveland Clinic), Benjamin L. Ebert(Dana-Farber Cancer Institute), Guillermo Garcia‐Manero(The University of Texas MD Anderson Cancer Center), Claudia Haferlach(Munich Leukemia Laboratory (Germany)), Torsten Haferlach(Munich Leukemia Laboratory (Germany)), Wolfgang Kern(Munich Leukemia Laboratory (Germany)), Seishi Ogawa(Kyoto University), Yasunobu Nagata(Cleveland Clinic), Kenichi Yoshida(Kyoto University), Timothy A. Graubert(Massachusetts General Hospital), Matthew J. Walter(Washington University in St. Louis), Alan F. List(Moffitt Cancer Center), Rami S. Komrokji(Moffitt Cancer Center), Eric Padron(Moffitt Cancer Center), David A. Sallman(Moffitt Cancer Center), Elli Papaemmanuil(Memorial Sloan Kettering Cancer Center), Peter J. Campbell(Wellcome Sanger Institute), Michael R. Savona(Vanderbilt University), Adam C. Seegmiller(Vanderbilt University), Lionel Adès(Délégation Paris 7), Pierre Fenaux(Délégation Paris 7), Lee‐Yung Shih(Chang Gung University), David Bowen(Leeds Teaching Hospitals NHS Trust), Michael J. Groves(University of Dundee), Sudhir Tauro(University of Dundee), Michaëla Fontenay(Université Paris Cité), Olivier Kosmider(Université Paris Cité), Michal Bar‐Natan(Icahn School of Medicine at Mount Sinai), David P. Steensma(Dana-Farber Cancer Institute), Richard M. Stone(Dana-Farber Cancer Institute), Michael Heuser(Medizinische Hochschule Hannover), Felicitas Thol(Medizinische Hochschule Hannover), Mario Cazzola(University of Pavia), Luca Malcovati(University of Pavia), Aly Karsan(University of British Columbia), Christina Ganster(University of Göttingen), Eva Hellström‐Lindberg(Karolinska University Hospital), Jacqueline Boultwood(University of Oxford), Andrea Pellagatti(University of Oxford), Valeria Santini(University of Florence), Lynn Quek(University of Oxford), Paresh Vyas(University of Oxford), Heinz Tüchler(Ludwig Boltzmann Institute for Cancer Research), Peter L. Greenberg(Stanford University), Rafael Bejar(University of California San Diego)
Leukemia
January 11, 2019
Cited by 256Open Access
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Abstract

Risk stratification is critical in the care of patients with myelodysplastic syndromes (MDS). Approximately 10% have a complex karyotype (CK), defined as more than two cytogenetic abnormalities, which is a highly adverse prognostic marker. However, CK-MDS can carry a wide range of chromosomal abnormalities and somatic mutations. To refine risk stratification of CK-MDS patients, we examined data from 359 CK-MDS patients shared by the International Working Group for MDS. Mutations were underrepresented with the exception of TP53 mutations, identified in 55% of patients. TP53 mutated patients had even fewer co-mutated genes but were enriched for the del(5q) chromosomal abnormality (p < 0.005), monosomal karyotype (p < 0.001), and high complexity, defined as more than 4 cytogenetic abnormalities (p < 0.001). Monosomal karyotype, high complexity, and TP53 mutation were individually associated with shorter overall survival, but monosomal status was not significant in a multivariable model. Multivariable survival modeling identified severe anemia (hemoglobin < 8.0 g/dL), NRAS mutation, SF3B1 mutation, TP53 mutation, elevated blast percentage (>10%), abnormal 3q, abnormal 9, and monosomy 7 as having the greatest survival risk. The poor risk associated with CK-MDS is driven by its association with prognostically adverse TP53 mutations and can be refined by considering clinical and karyotype features.


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