A complex chromosome rearrangement present in a B-cell line established from a patient with Burkitt lymphoma was studied by using fluorescence in situ hybridization (FISH) and immunocytochemistry techniques. The rearranged chromosome (der17) was apparently composed of 17q, of a partially deleted 17p, and of other material of chromosome 17p origin that was interspersed with regions without any clear banding pattern. der(17) contained a functional ch17 centromere and two additional centromeres of unknown origin that were inactive by all evidence. By FISH analysis with a TP53 probe, a signal could be demonstrated on the normal ch17, but not on the rearranged chromosome, a finding which indicates that 17p deletion caused a concurrent loss of one of the two TP53 alleles. The marker chromosome was previously observed in some of the malignant cells obtained from the patient's peripheral blood. These observations therefore indicate that cells with this specific rearrangement were generated in vivo and subsequently selected. This rearrangement is likely to have conferred a selective growth advantage to a subclone present in the original malignant cell population.