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References
Pui C-H, Carroll WL, Meshinchi S, Arceci RJ . Biology, risk stratification, and therapy of pediatric acute leukemias: an update. J Clin Oncol 2011; 29: 551–565.
Zwaan CM, Kolb E a, Reinhardt D, Abrahamsson J, Adachi S, Aplenc R et al. Collaborative efforts driving progress in pediatric acute myeloid leukemia. J Clin Oncol 2015; 33: 2949–2962.
Gough SM, Slape CI, Aplan PD . NUP98 gene fusions and hematopoietic malignancies: Common themes and new biologic insights. Blood 2011; 118: 6247–6257.
de Rooij JDE, Hollink IH, Arentsen-Peters ST, van Galen JF, Berna Beverloo H, Baruchel A et al. NUP98/JARID1A is a novel recurrent abnormality in pediatric acute megakaryoblastic leukemia with a distinct HOX gene expression pattern. Leukemia 2013; 27: 2280–2288.
Hollink IH, van den Heuvel-Eibrink MM, Arentsen-Peters ST, Pratcorona M, Abbas S, Kuipers JE et al. NUP98/NSD1 characterizes a novel poor prognostic group in acute myeloid leukemia with a distinct HOX gene expression pattern. Blood 2011; 118: 3645–3656.
Gough SM, Lee F, Yang F, Walker RL, Zhu YJ, Pineda M et al. NUP98-PHF23 is a chromatin-modifying oncoprotein that causes a wide array of leukemias sensitive to inhibition of PHD histone reader function. Cancer Discov 2014; 4: 564–577.
Pigazzi M, Manara E, Bisio V, Aveic S, Masetti R, Menna G et al. Screening of novel genetic aberrations in pediatric acute myeloid leukemia: A report from the AIEOP AML-2002 study group. Blood 2012; 120: 3860–3862.
Struski S, Lagarde S, Bories P, Puiseux C, Prade N, Cuccuini W et al. NUP98 is rearranged in 3.8% of pediatric AML forming a clinical and molecular homogenous group with a poor prognosis. Leukenia 2017; 31: 565–572.
Pession A, Masetti R, Rizzari C, Putti MC, Casale F, Fagioli F et al. Results of the AIEOP AML 2002/01 multicenter prospective trial for the treatment of children with acute myeloid leukemia. Blood 2013; 122: 170–178.
Masetti R, Pigazzi M, Togni M, Astolfi A, Indio V, Manara E et al. CBFA2T3-GLIS2 fusion transcript is a novel common feature in pediatric, cytogenetically normal AML, not restricted to FAB M7 subtype. Blood 2013; 121: 3469–3472.
Manara E, Basso G, Zampini M, Buldini B, Tregnago C, Rondelli R et al. Characterization of children with FLT3ITD acute myeloid leukemia: a report from the AIEOP AML2002 study group. Leukemia 2017; 31: 18–25.
Salsi V, Ferrari S, Gorello P, Fantini S, Chiavolelli F, Mecucci C et al. NUP98 fusion oncoproteins promote aneuploidy by attenuating the mitotic spindle checkpoint. Cancer Res 2014; 74: 1079–1090.
De Rooij JDE, Masetti R, Van Den Heuvel-Eibrink MM, Cayuela JM, Trka J, Reinhardt D et al. Recurrent abnormalities can be used for risk group stratification in pediatric AMKL: a retrospective intergroup study. Blood 2016; 127: 3424–3430.
Pigazzi M, Manara E, Bresolin S, Tregnago C, Beghin A, Baron E et al. MicroRNA-34b promoter hypermethylation induces CREB overexpression and contributes to myeloid transformation. Haematologica 2013; 98: 602–610.
Mitton B, Chae H-D, Hsu K, Dutta R, Aldana-Masangkay G, Ferrari R et al. Small molecule inhibition of cAMP response element binding protein in human acute myeloid leukemia cells. Leukemia 2016; 30: 2302–2311.
Acknowledgements
This work was supported by grants from Università degli Studi di Padova and by CARIPARO Istituto di Ricerca Pediatrica-Fondazione Città della Speranza to VB, CT, AL, GB, MP MZ, EM, ADM, GB and by grants from AIRC (Associazione Italiana Ricerca sul Cancro, Special Grant “5xmille”-9962), Ministero della Salute (RF-2010-2316606) to F. Locatelli. We thank Katia Polato for technical assistance. Plasmids used in the screening were kindly provided by Peter D. Aplan and Keith R. Humphries.
Author contributions
VB, EM, CT, VS, DDG, MT, performed in vitro experiments; MZ performed GEP analysis; AL, ADM, CM, VZ performed and interpreted cytogenetic analysis; SM performed xenotransplantation in NSG mice; RR, EM, RM performed the statistical analysis; FL, GB, MP designed the research, analyzed and interpreted data, wrote the manuscript.
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Bisio, V., Zampini, M., Tregnago, C. et al. NUP98-fusion transcripts characterize different biological entities within acute myeloid leukemia: a report from the AIEOP-AML group. Leukemia 31, 974–977 (2017). https://doi.org/10.1038/leu.2016.361
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DOI: https://doi.org/10.1038/leu.2016.361
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