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Genomic Profiling of Pediatric ALK-Positive Anaplastic Large Cell Lymphoma: A Children's Cancer and Leukaemia Group Study

Lookup NU author(s): Dr Christopher Bacon

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Abstract

Anaplastic lymphoma kinase (ALK)-positive anaplastic large cell lymphoma (ALCL) is a T-cell malignancy in which ALK expression is a consequence of the t(2;5) or a variant translocation involving Chromosome 2. For the most part, this disease presents in the pediatric population and most, but not all, patients are successfully treated. Although the t(2;5) product nucleophosmin-ALK has been extensively studied for its transforming properties, very little is known regarding cooperative genetic mutations that may contribute to lymphomagenesis and may predict survival outcome, specifically in a purely pediatric population. We set out to determine the frequency and positions of genomic imbalances in this relatively rare disease. We collected biopsy material from 15 UK-resident children with ALK-expressing ALCL. We performed array comparative genomic hybridization at a resolution of 1 MB using DNA isolated from tumor tissue. Some of the more common genomic gains were confirmed by quantitative PCR. Regions of genomic gain were far more common than losses and were most often detected on chromosomes 1-4, 5-12, 14, and 17, with Chromosome I I being the most frequent site of genomic imbalances. Patients with 14 or fewer imbalances had a lower overall 3-year survival (87.5-40%, P = 0.14) as did patients with gains in the regions of DDBI or BIRCS. A range of genomic imbalances exist in ALK-expressing ALCL of a pediatric origin, with a greater number associated with poorer overall survival. (C) 2009 Wiley-Liss, Inc.

Publication metadata

Author(s): Youssif C, Goldenbogen J, Hamoudi R, Carreras J, Viskaduraki M, Cui YX, Bacon CM, Burke GAA, Turner SD

Publication type: Article

Publication status: Published

Journal: Genes, Chromosomes & Cancer

Year: 2009

Volume: 48

Issue: 11

Pages: 1018-1026

ISSN (print): 1045-2257

ISSN (electronic): 1098-2264

Publisher: John Wiley & Sons, Inc.

URL: http://dx.doi.org/10.1002/gcc.20701

DOI: 10.1002/gcc.20701

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