The constitutively activated tyrosine kinase activity of the p210bcr-abl fusion protein, generated by a t(9;22)(q34;q11) chromosomal translocation, is pathogenetically associated with chronic myeloid leukemia (CML). However, mechanisms contributing to the expansion of a BCR-ABL positive clone are largely obscure. In the presence of an impaired immune surveillance, cells carrying any of these alterations may become phenotypically relevant. Therefore, immunosuppressed solid organ recipients represent an optimal population to investigate the frequency of mRNA products of this translocation. Blood leukocytes were studied in 201 individuals (100 organ recipients and 101 control individuals) for the presence of BCR-ABL transcripts by a nested-reverse transcriptase-polymerase chain reaction assay, routinely used in our institution. In 5/100 immunosuppressed patients, at least one out of two RT-PCR products was bcr-abl positive while all controls were negative. These findings were extended by four CML cases of organ transplant recipients (three renal and one liver transplants). Three of these cases developed CML in a total of 2088 transplantations in 9 yr, suggesting a higher incidence of CML in these patients.