Specific genomic alterations may be involved in the transformation of a normal cell to a malignant one (Nowell, 1986). Characteristic translocations, often related to cellular oncogenes, are frequent in B-non-Hodgkin's lymphoma (B-NHL). In Burkitt's lymphoma, a translocation t(8; 14) activates the c-myc oncogene and in 85% of follicular lymphomas a translocation t(14; 18) is detected, involving the putative oncogene bcl-2 (Dalla Favera et al., 1982; Tsujimoto et al., 1985). The clonal evolution of B-NHL is marked by successive chromosomal changes (Yunis et al., 1987), some of which correlate with histologic signs of progression and a more malignant course of the disease (Koduru et al., 1987). Karyotype analysis, however, is technically difficult in solid tumours and impossible in cases where only frozen tissue is available. By detecting a large amount of chromosomal loci dispersed throughout the genome, minisatellite probes may serve as probes for chromosomal changes (Jeffreys et al., 1985). Thein et al. used this approach to screen the DNA of 35 patients with a variety of cancers and found differences between the constitutional DNA and tumour DNA in ten cases (Thein et al., 1987). The changes were interpreted as either unequal sister-chromatid exchanges producing new fragments, or variations in fragment intensity and hence chromosomal copy number. Using minisatellite probe 33.15, we studied two EBV-negative cell lines, HH2 and HH3, derived from pleural effusion cells of a single B-immunoblastic NHL. In parallel, karyotype analysis was performed to relate the changes seen in DNA-fingerprint directly to cytogenetic differences. Cell line HH2 and the original malignant pleural effusion cells showed 48XY + 7 +dell2(q24) t(14; 18)(q32; q21). Cell line HH3 showed the same karyotype except that no partial trisomy 12 was present. On hybridizing to the minisatellite probe 33.15, the fingerprints of cell lines HH2 and HH3 and of the original tumour were indistinguishable, but for 5.1 and 2.7kb fragments present in HH2 and in the original tumour and absent in HH3 (Figure 1). This finding suggests the location of