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Abstract
The pre-B-cell (clgM) phenotype of childhood ALL comprises about one-fifth of newly diagnosed cases. It has a high frequency of chromosomal translocation, and is closely associated with the t(l;19)(q23;p13). The poor treatment outcome and high-risk features previously ascribed to this phenotype appear to be primarily due to the subset of cases with the t(l;19). Early results of at least one study suggest that aggressive treatment may even nullify the adverse prognostic implication of the t(l;19). Finally, molecular analyses of these cases have yielded exciting new information regarding the pathogenesis of pre-B-cell ALL with the t(l;19), and recombinant DNA technology (polymerase chain reaction) is likely to make molecular diagnosis and detection of minimal residual disease possible in the near future.