The role of chromosomal translocations in B- and T-cell neoplasia.

At the turn of the century, Boveri (1) suggested that abnormal chro­ mosomal patterns in tumor samples reflect the processes responsible for the development of the malignant phenotype. However, the first demonstrated association of a consistent chromosomal rearrangement with a specifi c disease did not occur until 1960 when a marker chromosome, the Phi­ ladelphia chromosome (Ph +), was discovered to be consistently associated with chronic myelogenous leukemia (CML) (2). The Ph+ chromosome was subsequently shown to result from a reciprocal translocation between chromosomes 9 and 22 (3). Due to the introduction of new techniques for "high resolution" ban­ ding-analysis of chromosomes, a large majority of human cancer cells are now known to carry clonal cytogenetic changes (4). This has been most clearly demonstrated for the hematopoietic malignancies and has resulted in a renewed focus on chromosomal rearrangements as a causative factor in malignant transformation. While this view was originally not widely accepted outside of the discipline of cytogenetics, the painstaking efforts to observe and catalogue these rearrangements have now been justifi ed. The application of the new technologies of molecular biology and somatic cell genetics have allowed the characterization of a variety of chromosomal abnormalities, and in particular chromosomal translocations, at the mol-

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