Produção Nacional
Revisado por pares
Molecular Characterization of Pediatric Acute Myeloid Leukemia: Results of a Multicentric Study in Brazil
2016; Elsevier BV; Volume: 47; Issue: 8 Linguagem: Inglês
10.1016/j.arcmed.2016.11.015
ISSN1873-5487
AutoresFrancianne Gomes Andrade, Elda Pereira Noronha, Gisele Dallapicola Brisson, Filipe V. dos Santos-Bueno, Ingrid Sardou Cezar, Eugênia Terra‐Granado, Luiz Cláudio Santos Thuler, Maria S. Pombo‐de‐Oliveira, Alejandro Mauricio Arancibia, Rosania Maria Basegio, Patricia Carneiro de Brito, Eny Carvalho, José Carlos Córdoba, Imaruí Costa, Virgínia Maria Cóser, Adriana Vanessa Santini Deyl, Anna Carolina Silva Dias, Eloisa Cartaxo Eloy Fialho, Bruno Marcelo Rocha Freire, Renata Silva de Carvalho Gurgel, Maura Rosane Valério Ikoma, Ingrid Köster, Isis Maria Quezado Magalhães, Ana Maria Marinho, Renato Melaragno, Suellen Valadares Moura, Gustavo Ribeiro Neves, Claudia Teresa de Oliveira, Ilana Zalcberg Renault, Terezinha de Jesus Marques-Salles, Denise Browsfield Silva, Marcelo Santos de Souza, Tállita Meciany Farias Vieira, Fernando de Almeida Werneck, Ana Freund Winn, G Zamperlini,
Tópico(s)Retinoids in leukemia and cellular processes
ResumoThe biological characterization of childhood acute myeloid leukemia (c-AML) is an important outcome predictor. In Brazil, very little is known about the frequency of AML subgroups, although c-AML accounts for about 18% of leukemias. We carried out this study to investigate the contribution of type I and II gene mutations in the probability of overall survival (pOS) of c-AML in Brazil. Seven hundred and three de novo pediatric AML cases (2000–2015) were assessed throughout a multicentric network study. Mutations in hotspot regions of FLT3, NRAS, KRAS, PTPN11, and c-KIT genes were analyzed as well as fusion genes (RUNX1-RUNX1T1, MLL/KMT2A-r, CBFβ-MYH11, and PML-RARα) associated with AML. Patients were treated out of the clinical trial although following the BFM-AML2004 protocol. Acute promyelocytic leukemia (APL) was treated differently. AML with Down syndrome was excluded. There were significant differences in gene mutations among age ranges (≤2 years-old; >2–10 years old and ≥11 years old) and the nonrandom association between type I/II mutations. Lower white blood cell count (≤50 × 109/L) was associated with RUNX1-RUNX1T1, whereas higher WBC with CBFβ-MYH11 (p <0.05). Cumulative pOS in 5 years was 37.7 ± 2.8% for total AMLs and 59.8 ± 6.2% for APL (p = 0.03). pOS differences were observed between Brazilian regions. The South-Southeast regions had a better 5-year pOS, whereas the Midwest region presented the poorest pOS (23.7 ± 4.9%). PTPN11 mutations conferred an adverse prognosis as an independent prognostic factor. Identification of genetic subgroups contributes to the molecular epidemiology and biology of AML worldwide, reflecting the profile of pediatric AML cases in Brazil.
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