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Blood, 15 August 2007, Vol. 110, No. 4, pp. 1112-1115.
Prepublished online as a Blood First Edition Paper on May 1, 2007; DOI 10.1182/blood-2006-07-038299.
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Submitted July 28, 2006
Accepted March 12, 2007
Outcome of treatment in children with hypodiploid acute lymphoblastic leukemia
James B Nachman*, Nyla A. Heerema, Harland Sather, Bruce Camitta, Erik Forestier, Christine J Harrison, Nicole Dastugue, Martin Schrappe, Ching-Hon Pui, Giuseppe Basso, Lewis B. Silverman, and Gritta E. Janka
University of Chicago Comer Children's Hospital, Chicago, IL, United States
Columbus Children's Hospital and The Ohio State University, Columbus, OH, United States
Operations Center, Children's Oncology Group, Arcadia, CA, United States
Midwest Children's Cancer Center, Dept of Pediatrics of the Medical College of Wisconsin, Children's Hospital of Wisconsin, Milwaukee, WI, United States
Department of Clinical Sciences and Paediatrics, University of Umea, Umea, Sweden
Leukaemia Research Cytogenetics Group, Cancer Sciences Division, University of Southampton, Southampton, United Kingdom
Genetique des Hemopathies, Laboratoire d'Hematologie, Hopital Purpan, Toulouse, France
Department of Pediatrics, University Hospital Schwanenweg, Kiel, Germany
St. Jude Children's Research Hospital, and the University of Tennessee Health Science Center, Memphis, TN, United States
Pediatrics Department, University of Padova, Padova, Italy
Department of Pediatric Oncology, Dana-Farber Cancer Institute & Division of Hematology Oncology, Children's Hospital, Boston, MA, United States
Department of Hematology and Oncology, Children's University Hospital, Hamburg, Germany
* Corresponding author; email: jnachman{at}peds.bsd.uchicago.edu.
One hundred and thirty-nine patients with acute lymphoblastic leukemia (ALL) and hypodiploidy (less than 45 chromosomes) were collected from 10 different national ALL study groups or single institutions. Patients were stratified by modal chromosome number into four groups: 24-29 (N=46); 33-39 (N=26); 40-43 (N=13) and 44 chromosomes (N=54). Nine patients were Philadelphia chromosome (Ph) positive (four cases - 44 chromosomes; five cases - 40-43 chromosomes) and were not considered further. Event-free survival (EFS) and overall survival (OS) of the remaining 130 patients were 38.5% ± 4.4% and 49.8% ± 4.2% at 8 years, respectively. There were no significant differences in outcome between patients with 24-29, 33-39, or 40-43 chromosomes. Compared to patients with <44 chromosomes, patients with 44 chromosomes had a significantly better EFS (P=.01; 8-year estimate, 52.2% vs 30.1%) and OS (P=.017; 69% vs 37.5%). For patients with 44 chromosomes, monosomy 7, the presence of a dicentric chromosome, or both predicted a worse EFS but similar OS. Doubling of the hypodiploid clone occurred in 32 patients (24-29 chromosomes (n=25) and 33-39 chromosomes (n=7)) and had no prognostic implication. Children and adolescents with ALL and hypodiploidy with less than 44 chromosomes have a poor outcome despite contemporary therapy.
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