The t(14;18) (q21;q32) translocation was originally identified as occurring in follicular low-grade non-Hodgkin’s lymphomas of B-cell origin in 1978 (1), and has been found in up to 85% of cases subsequently (2 –4 ). The translocation appears to arise at the pre-B-cell stage in the bone marrow when VDJ recombination usually occurs (5 ), so that the Bcl-2 gene on chromosome 18 is connected to the 5′ end of one of the six JH segments of the immunoglobulin heavy chain locus on chromosome 14 (6 ). The result of this is the constitutional upregulation ofBcl-2 expression (7 , 8 ), which results in the suppression of apoptotic cell death among the population carrying the abnormality (9 ). It is suggested that this disrupts the normal process by which B-cell clones are eliminated during affinity maturation in germinal centers (10 ), thereby giving rise to an expanded B-lymphocyte pool in which further lymphomagenic events can supervene.
