The most common translocation in non-Hodgkin lymphomas (NHL) is a t(14;18)(q32;q21) recombining the immunoglobulin heavy-chain gene (IGH) on chromosome 14 with the B cell leukemia/lymphoma 2 (BCL2) gene on chromosome 18. Although NHLs carrying a t(14;18) typically begin as low-grade, follicular lymphomas, they have a tendency towards transformation to more aggressive disease, something that is accompanied, presumably caused, by the acquisition of secondary chromosomal changes. One such common change is add(1)(p36), in which material of unknown origin is added to the tip of the short arm of chromosome 1. We used multicolor fluorescence in situ hybridization (M-FISH), a new FISH-based screening technique, to better characterize the rearrangement. Whenever doubt persisted after M-FISH, hybridization with chromosome-specific probes was also performed. In 5 out of 14 informative cases, the extra material on 1p36 could be shown to have come from 17q, more specifically 17q11-21 --> qter, whereas it came from 6p and 11q in two cases each and from 3p, 8p, 8q, 9q, and 12p in one case each. It appears, therefore, that der(1)t(1;17)(p36;q11-21) is a common secondary aberration in NHLs with t(14;18) as the primary abnormality, accounting for about one-third of all add(1)(p36) chromosomes seen in this cytogenetic subset.