Editorial The next step for Burkitt lymphoma

The successes in the treatment of childhood acute lymphoblastic leukemia (ALL) are well known, with a cure rate of more than 80% of patients treated. However, for the minority of patients who fail to achieve long-term remission, treatment options are limited with overall poor prognosis. Much the same can be said for Burkitt lymphoma today, once considered in the same disease category as precursor B ALL and erroneously treated in a similar manner. The major characteristics of Burkitt lymphoma are well established; morphologically, Burkitt lymphoma consists of a homogenous population of medium-sized cells with a high mitotic rate [1]. Immunophenotype spectrum includes expression of surface IgM, CD19, CD20, CD22, CD10, CD79a, and negative results for TdT [2]. Above all, important corroborating evidence for the diagnosis of Burkitt lymphoma includes translocations involving the MYC gene at locus 8q24. These MYC translocations consist of t(8;14)(q24;q32), by far the most common, and t(8;22)(q24;q11) and t(2;8) (p12;p24) to a much lesser extent, all of which result in the realignment of the MYC oncogene with immunoglobulin promoter/enhancer elements. Tumor lysis syndrome is an important complication th at requires meticulous attention during the early phases of treatment. All of these traits also apply to ALL, L3 and the two entities are now considered to represent different aspects of the same disease.