In myeloid and lymphoid leukemias recurrent chromosomal aberrations can be detected in chromosome region 12pl3. We characterized the genes involved in t (12; 22)(pl3; qll) in two patients with myeloid leukemia and one with myelodysplasia syndrome (MDS). MN1, a gene on chromosome 22< ill was shown to be fused to TEL, a member of the family of ETS transcription factors on chromosome 12pl3. The translocation results in transcription of the reciprocal fusion mRNAs, MN1-TEL and TKL-MN1, of which MNÍ-TEL is likely to encode an aberrant transcription factor containing the ETS DNA-binding domain of TEL. In addition to fusion of TEL to the PDGE/Í receptor in t (5; 12) in chronic myelomonocytic leukemia (CMML), our data suggest that the involvement of this protein in myeloid leukemogenesis could be dual; its isolated proteinprotein dimeri/. ation and DNA-binding domains may be crucial for the oncogenic activation of functionally different fusion proteins.