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Luque Paz, Damien; Riou, Jérémie; Verger, Emmanuelle; Cassinat, Bruno; Chauveau, Aurélie; Ianotto, Jean-Christophe; Dupriez, Brigitte; Boyer, Françoise; Renard, Maxime; Mansier, Olivier; Murati, Anne; Rey, Jérôme; Etienne, Gabriel; Mansat-De Mas, Véronique; Tavitian, Suzanne; Nibourel, Olivier; Girault, Stéphane; Le Bris, Yannick; Girodon, François; Ranta, Dana; Chomel, Jean-Claude; Cony-Makhoul, Pascale; Sujobert, Pierre; Robles, Margot; Ben Abdelali, Raouf; Kosmider, Olivier; Cottin, Laurane; Roy, Lydia; Sloma, Ivan; Vacheret, Fabienne; Wemeau, Mathieu; Mossuz, Pascal; Slama, Borhane; Cussac, Vincent; Denis, Guillaume; Walter-Petrich, Anouk; Burroni, Barbara; Jézéquel, Nathalie; Giraudier, Stéphane; Lippert, Eric; Socié, Gérard; Kiladjian, Jean-Jacques; Ugo, Valérie
Blood advances, 03/2021, Letnik: 5, Številka: 5Journal Article
We aimed to study the prognostic impact of the mutational landscape in primary and secondary myelofibrosis. The study included 479 patients with myelofibrosis recruited from 24 French Intergroup of Myeloproliferative Neoplasms (FIM) centers. The molecular landscape was studied by high-throughput sequencing of 77 genes. A Bayesian network allowed the identification of genomic groups whose prognostic impact was studied in a multistate model considering transitions from the 3 conditions: myelofibrosis, acute leukemia, and death. Results were validated using an independent, previously published cohort (n = 276). Four genomic groups were identified: patients with TP53 mutation; patients with ≥1 mutation in EZH2, CBL, U2AF1, SRSF2, IDH1, IDH2, NRAS, or KRAS (high-risk group); patients with ASXL1-only mutation (ie, no associated mutation in TP53 or high-risk genes); and other patients. A multistate model found that both TP53 and high-risk groups were associated with leukemic transformation (hazard ratios HRs 95% confidence interval, 8.68 3.32-22.73 and 3.24 1.58-6.64, respectively) and death from myelofibrosis (HRs, 3.03 1.66-5.56 and 1.77 1.18-2.67, respectively). ASXL1-only mutations had no prognostic value that was confirmed in the validation cohort. However, ASXL1 mutations conferred a worse prognosis when associated with a mutation in TP53 or high-risk genes. This study provides a new definition of adverse mutations in myelofibrosis with the addition of TP53, CBL, NRAS, KRAS, and U2AF1 to previously described genes. Furthermore, our results argue that ASXL1 mutations alone cannot be considered detrimental. •Mutations of TP53 and high-risk genes (EZH2, CBL, U2AF1, SRSF2, IDH1, IDH2, NRAS or KRAS) are adverse prognostic factors in myelofibrosis.•ASXL1 isolated mutations (ie, without TP53 or high-risk mutations) have no prognostic impact in myelofibrosis. Display omitted
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JCR | SNIP | JCR | SNIP | JCR | SNIP | JCR | SNIP |
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Vir: Osebne bibliografije
in: SICRIS
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