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Racial Differences in the Survival of Childhood B-Precursor Acute Lymphoblastic Leukemia: A Pediatric Oncology Group Study

From the University of Florida, and Pediatric Oncology Group Statistical Office, Gainesville, FL; Washington University, St Louis, MO; Midwest Children’s Cancer Center, and Children’s Hospital of Wisconsin, Medical College of Wisconsin, Milwaukee, WI; Children’s Hospital of Michigan, and Wayne State University, Detroit, MI; University of Mississippi School of Medicine, Jackson, MS; Children’s Memorial Hospital, and Pediatric Oncology Group Operations Office, Chicago, IL; Baylor College of Medicine, Houston, TX; and Emory University, Atlanta, GA.

Address reprint requests to Brad H. Pollock, MPH, PhD, Pediatric Oncology Group Statistical Office 104 North, Main St, Suite 600, Gainesville, FL 32601-3330; email brad{at}pog.ufl.edu

PURPOSE: We conducted a historic cohort study to test the hypothesis that, after adjustment for biologic factors, African-American (AA) children and Spanish surname (SS) children with newly diagnosed B-precursor acute lymphoblastic leukemia had lower survival than did comparable white children.

PATIENTS AND METHODS: From 1981 to 1994, 4,061 white, 518 AA, and 507 SS children aged 1 to 20 years were treated on three successive Pediatric Oncology Group multicenter randomized clinical trials.

RESULTS: AA and SS patients were more likely to have adverse prognostic features at diagnosis and lower survival than were white patients. The 5-year cumulative survival rates were (probability ± SE) 81.9% ± 0.6%, 68.6% ± 2.1%, and 74.9% ± 2.0% for white, AA, and SS children, respectively. Adjusting for age, leukocyte count, sex, era of treatment, and leukemia blast cell ploidy, we found that AA children had a 42% excess mortality rate compared with white children (proportional hazards ratio [PHR] = 1.42; 95% confidence interval [CI], 1.12 to 1.80), and SS children had a 33% excess mortality rate compared with white children (PHR = 1.33; 95% CI, 1.19 to 1.49).

CONCLUSION: Clinical presentation, tumor biology, and deviations from prescribed therapy did not explain the differences in survival and event-free survival that we observed, although differences seem to be diminishing over time with improvements in therapy. The disparity in outcome for AA and SS children is most likely related to variations in chemotherapeutic response to therapy and not to compliance. Further improvements in outcome may require individualized dosing based on specific pharmacogenetic profiles, especially for AA and SS children.

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