CD44 deficiency is a consistent finding in childhood Burkitt's lymphoma and leukemia

Abstract

B-cell-derived non-Hodgkin's lymphoma (NHL) of childhood and adolescence can be subdivided into mature B-cell neoplasms and B-cell precursor (BCP) lymphoblastic lymphomas (LBL). The former comprise Burkitt's lymphoma and leukemia, diffuse large B-cell lymphoma (DLBCL) and primary mediastinal large B-cell lymphoma. With adequate therapy, about 80–90% of the patients with mature B-cell malignancies can now become long-term, disease-free survivors.1 However, the prognosis of children who suffer from a relapse is still very poor. In most therapy studies, risk stratification for mature B-cell NHL is largely based on stage of disease and the initial serum lactate dehydrogenase level.1 Moreover, to date, evaluation of minimal disseminated disease (MDD) at the time of diagnosis, that is in the bone marrow (BM) or peripheral blood, and of the kinetics of minimal residual disease (MRD) have not yet been implemented into the risk assignment of modern protocols. Nevertheless, as Burkitt's lymphoma is genetically characterized by the presence of a chromosomal translocation involving the C-MYC oncogene on chromosome 8 and one of the loci of the immunoglobulin (Ig) heavy- or light-chain genes on chromosomes 14, 22 or 2, the molecular fusion products have been explored in a few polymerase chain reaction (PCR)-based studies to assess both minimal disseminated and residual diseases.2, 3 However, considering the long-time experience of different techniques on MRD analysis in childhood acute lymphoblastic leukemia (ALL), it seems very likely that besides PCR-based examinations of disease-specific fusion genes or clone-specific Ig gene rearrangements, flow cytometry could also allow MDD and MRD detection in Burkitt's malignancies.4, 5