Dic(9;20)(p13;q11) in childhood acute lymphoblastic leukaemia is related to low cellular resistance to asparaginase, cytarabine and corticosteroids.

Abstract

To access publisher full text version of this article. Please click on the hyperlink in Additional Links fieldDic(9;20)(p13;q11) was first described as a nonrandom chromosome abnormality in B-cell precursor acute lymphoblastic leukaemia (BCP ALL) in the mid 1990s,1, 2 and 71 dic(9;20)-positive cases have since then been reported.3, 4, 5 Approximately 90% of these cases were children or adolescents, with dic(9;20) occurring in about 2% of childhood BCP ALL.6 The recent review by Forestier et al.5 describes that dic(9;20)-leukaemias are of B-cell precursor immunophenotype, never have a high hyperdiploid modal number, show a female predominance, and have a significant age incidence peak at 3 years. Most patients are allocated to non-standard risk treatment arms due to high WBC (median 24 109/l) and a relatively high frequency of CNS disease or other extra-medullary leukaemia (EML) at diagnosis. The prognostic implications of dic(9;20) are to a large extent unknown. A relatively large proportion of the relapses reported in the literature have been extra-medullary, and post-relapse treatment including block therapy has been successful in several patients, as illustrated by a p-EFS of 0.62 and a predicted overall survival of 0.82 at 5 years for the 24 Nordic cases.