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Blood, 15 October 2003, Vol. 102, No. 8, pp. 3010-3015.
Prepublished online as a Blood First Edition Paper on June 26, 2003; DOI 10.1182/blood-2003-05-1444.
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NEOPLASIA
Formation of trisomies and their parental origin in hyperdiploid childhood acute lymphoblastic leukemia
Kajsa Paulsson,
Ioannis Panagopoulos,
Sakari Knuutila,
Kowan Ja Jee,
Stanislaw Garwicz,
Thoas Fioretos,
Felix Mitelman, and
Bertil Johansson
From the Department of Clinical Genetics, Lund University Hospital, Sweden; the Departments of Pathology and Medical Genetics, Haartman Institute and Helsinki University Central Hospital, University of Helsinki, Finland; and the Department of Pediatrics, Lund University Hospital, Sweden.
High hyperdiploidy, common in childhood acute lymphoblastic leukemia (ALL) with a favorable prognosis, is characterized by specific trisomies. Virtually nothing is known about its formation or pathogenetic impact. We evaluated 10 patients with ALL using 38 microsatellite markers mapped to 18 of the 24 human chromosomes to investigate the mechanisms underlying hyperdiploidy and to ascertain the parental origin of the trisomies. Based on the results, doubling of a near-haploid clone and polyploidization with subsequent losses of chromosomes could be excluded. The finding of equal allele dosage for tetrasomy 21 suggests that hyperdiploidy originates in a single aberrant mitosis, though a sequential gain of chromosomes other than 21 in consecutive cell divisions remains a possibility. Our study, the first to address experimentally the parental origin of trisomies in ALL, revealed no preferential duplication of maternally or paternally inherited copies of X, 4, 6, 9, 10, 17, 18, and 21. Trisomy 8 was of paternal origin in 4 of 4 patients (P = .125), and +14 was of maternal origin in 7 of 8 patients (P = .0703). Thus, the present results indicate that imprinting is not pathogenetically important in hyperdiploid childhood ALL, with the possible exception of the observed parental skewness of +8 and +14.
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No evidence for preferential maternal origin of duplicated chromosome 14 in hyperdiploid ALL
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