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Blood, 15 July 2006, Vol. 108, No. 2, pp. 711-717.
Prepublished online as a Blood First Edition Paper on March 28, 2006; DOI 10.1182/blood-2006-02-002824.
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NEOPLASIA
Biologic pathways associated with relapse in childhood acute lymphoblastic leukemia: a Children's Oncology Group study
Deepa Bhojwani,
Huining Kang,
Naomi P. Moskowitz,
Dong-Joon Min,
Hokyung Lee,
Jeffrey W. Potter,
George Davidson,
Cheryl L. Willman,
Michael J. Borowitz,
Ilana Belitskaya-Levy,
Stephen P. Hunger,
Elizabeth A. Raetz, and
William L. Carroll
From the New York University (NYU) Cancer Institute and Division of Pediatric Hematology/Oncology, New York, NY; Department of Biostatistics, NYU School of Medicine, New York, NY; Department of Pediatrics, Mount Sinai School of Medicine, New York, NY; The Cancer Research and Treatment Center, University of New Mexico, Albuquerque, NM; Sandia National Laboratories, Albuquerque, NM; Department of Pediatrics, University of Florida College of Medicine and the University of Florida Shands Cancer Center, Gainesville, FL; and the Department of Pathology and Oncology, Johns Hopkins Medical Institutions, Baltimore, MD.
Outcome for children with childhood acute lymphoblastic leukemia (ALL) who relapse is poor. To gain insight into the mechanisms of relapse, we analyzed gene-expression profiles in 35 matched diagnosis/relapse pairs as well as 60 uniformly treated children at relapse using the Affymetrix platform. Matched-pair analyses revealed significant differences in the expression of genes involved in cell-cycle regulation, DNA repair, and apoptosis between diagnostic and early-relapse samples. Many of these pathways have been implicated in tumorigenesis previously and are attractive targets for intervention strategies. In contrast, no common pattern of changes was observed among late-relapse pairs. Early-relapse samples were more likely to be similar to their respective diagnostic sample while we noted greater divergence in gene-expression patterns among late-relapse pairs. Comparison of expression profiles of early- versus late-relapse samples indicated that early-relapse clones were characterized by overexpression of biologic pathways associated with cell-cycle regulation. These results suggest that early-relapse results from the emergence of a related clone, characterized by the up-regulation of genes mediating cell proliferation. In contrast, late relapse appears to be mediated by diverse pathways.
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