Abnormalities of chromosome bands 13q12 to 13q14 in childhood acute lymphoblastic leukemia

Heerema, N.A.; Sather, H.N.; Sensel, M.G.; Lee, M.K.; Hutchinson, R.J.; Nachman, J.B.; Reaman, G.H.; Lange, B.J.; Steinherz, P.G.; Bostrom, B.C.; Gaynon, P.S.; Uckun, F.M.

Journal of Clinical Oncology Official Journal of the American Society of Clinical Oncology 18(22): 3837-3844


ISSN/ISBN: 0732-183X
PMID: 11078497
DOI: 10.1200/jco.2000.18.22.3837
Accession: 010111566

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Purpose: Little is known about nonrandom deletions of chromosome bands 13q12 to 13q14 (13q12-14) in acute lymphoblastic leukemia (ALL). We determined the prognostic significance of cytogenetically identified breakpoints in 13q12-14 in children with newly diagnosed ALL treated on Children's Cancer Group protocols from 1988 to 1995. Patients and Methods: Breakpoints in 13q12-14 were identified in 36 (2%) of the 1,946 cases with accepted cytogenetic data. Outcome analysis used standard life-table methods. Results: Seventeen patients (47%) with an abnormal 13q12-14 were classified, according to the National Cancer Institute (NCI), as poor risk, and 15 patients (42%) were standard risk; four (11%) were infants less than 12 months of age. Eight cases had balanced rearrangements of 13q12-14, 27 patients had a partial loss of 13q, and one had both a partial gain and a partial loss. The most frequent additional abnormalities among these patients were an abnormal 12p, a del(6q), a del(9p), a 14q11 breakpoint, and an 11q23 breakpoint. Nineteen patients were pseudodiploid, 10 were hyperdiploid, and seven were hypodiploid. Patients with an abnormal 13q12-14 had significantly worse event-free survival than patients lacking such an abnormality, with estimates at 6 years of 61% (SD = 14%) and 74% (SD = 1%), respectively (P = .04; relative risk = 1.74). Overall survival, however, was similar for the two groups (P = .25). The prognostic effect of an abnormal 13q was attenuated in a multivariate analysis adjusted for NCI risk status and ploidy (P = .72). Conclusion: Aberrations of 13q12-14 may contribute to leukemogenesis of childhood ALL and confer increased risk of treatment failure but are associated with other poor-risk features.