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Blood, 15 August 2005, Vol. 106, No. 4, pp. 1419-1422.
Prepublished online as a Blood First Edition Paper on May 3, 2005; DOI 10.1182/blood-2005-03-0899.
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NEOPLASIA
Brief report
Nucleophosmin mutations in childhood acute myelogenous leukemia with normal karyotype
Giovanni Cazzaniga,
Maria Grazia Dell'Oro,
Cristina Mecucci,
Emanuela Giarin,
Riccardo Masetti,
Vincenzo Rossi,
Franco Locatelli,
Massimo F. Martelli,
Giuseppe Basso,
Andrea Pession,
Andrea Biondi, and
Brunangelo Falini
From the University of Milan-Bicocca, Pediatric Clinic, M. Tettamanti Research Center, San Gerardo Hospital, Monza, Italy; the University of Perugia, Institute of Hematology, Perugia, Italy; the University of Padua, Pediatric Clinic, Onco-Hematology, Padova, Italy; the University of Bologna, Institute of Hematology and Medical Oncology Seragnoli, Bologna, Italy; and the Paediatric Haematology and Oncology, Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS) Policlinico San Matteo, Pavia, Italy.
Nucleophosmin (NPM) is a nucleocytoplasmic shuttling protein involved in leukemia-associated chromosomal translocations, and it regulates the alternate reading frame (ARF)-p53 tumorsuppressor pathway. Recently, it has been demonstrated that mutations of the NPM1 gene alter the protein at its C-terminal, causing its cytoplasmic localization. Cytoplasmic NPM was detected in 35% of adult patients with primary non-French-American-British (FAB) classification M3 acute myeloid leukemia (AML), associated mainly with normal karyotype. We evaluated the prevalence of the NPM1 gene mutation in non-M3 childhood AML patients enrolled in the ongoing Associazione Italiana di Ematologia e Oncologia Pediatrica (AIEOP-AML02) protocol in Italy. NPM1 mutations were found in 7 (6.5%) of 107 successfully analyzed patients. NPM1- mutated patients carried a normal karyotype (7/26, 27.1%) and were older in age. Thus, the NPM1 mutation is a frequent abnormality in AML patients without known genetic marker; the mutation may represent a new target to monitor minimal residual disease in AML and a potential candidate for alternative and targeted treatments. (Blood. 2005;106:1419-1422)
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