Dear Editor, The analysis of chromosomal translocations and the detection of fusion transcripts as a result of a translocation gave new insights in the understanding of the development of haematological disorders and targeted treatments. An example is the PDGFRβ gene located at 5q33 that forms fusion transcripts with several different partner genes [1]. All partner proteins contain putative dimerization motifs leading to dimerization of PDGFRβ and ligand-independent activation of the kinase domain. We, herein, report a patient with chronic myelomonocytic leukaemia (CMML) showing a translocation t(5;10) (q33;q22) in 21 of 22 analysed cells. Real-time polymerase chain reaction (RT-PCR) for BCR-ABL was negative. This, together with the clinical parameters, led to the diagnosis of CMML, belonging to the group of mixed myeloproliferative/myelodysplastic diseases according to the WHO classification, and we started a treatment with 400 mg of imatinib per day. Fourteen days later, white blood cell count normalized (4,600/μl). One month later, the other blood values, including haemoglobin, differential count and lysozyme, returned to normal as well. Five months after, beginning with imatinib treatment, both histological and cytological bone marrow examination showed a remission of the disease. To study whether the PDGFR gene was affected by the translocation, a fluorescence in situ hybridization analysis with BAC probes flanking the PDGFR gene was performed showing a disruption of this gene. Four further cases with a t(5;10)(q33;q22) have been described, all resulting in the formation of a fusion transcript between PDGFRβ and the H4/D10S170 gene at 10q22. To test whether these two genes were involved in our patient, a RT-PCR with specific primers to detect a fusion transcript was performed. Sequence analysis of the resulting PCR product showed the presence of a fusion transcript with exactly identical breakpoints at the cDNA level as described in all four previously published cases [2–5]. Figure 1a shows the sequence at the site of the fusion and the translocation occurring in intron 7 of the H4 gene and intron 10 of the PDGFRβ gene. In the following 2 years, the patient was monitored continuously clinically, cytogenetically and with molecular methods (Fig. 1b). The fusion transcript was only observed before imatinib treatment, and none of the remission samples were positive in the RT-PCR. At 5 months of treatment, a bone marrow and blood sample were analysed, and both were negative. All other analyses were from blood samples. The patient continues on imatinib, which is well tolerated besides gastrointestinal side effects and periorbital oedema, and the patient is still in complete haematological, cytological, chromosomal and molecular remission in November 2006. The description of patients with translocations involving the PDFGRβ gene and treatment with imatinib is important to evaluate the long-term effects. There was one report of a patient with a t(5;10) who did not respond, although a mutation in the kinase domain could Ann Hematol (2007) 86:353–354 DOI 10.1007/s00277-006-0247-5