Dermatofibrosarcoma protuberans (DP), an infiltrative skin tumour of intermediate malignancy¹, presents specific features such as reciprocal translocations t(17;22)(q22;q13) and supernumerary ring chromosomes derived from the t(17;22)^2,3. In this report, the breakpoints from translocations and rings in DP and its juvenile form, giant cell fibroblastoma (GCF)^4,5, were characterised on the genomic and RNA level. These rearrangements fuse the platelet-derived growth factor B-chain (PDGFB, c-sis proto-oncogene) and the collagen type I α1 (COL1A1) genes. PDGFB has transforming activity and is a potent mitogen for a number of cell types, but its role in oncogenic processes is not fully understood^6,7. COL1A1 is a major constituent of the connective tissue matrix8. Neither PDGFB nor COL1A1 have so far been implicated in any tumour translocations. These gene fusions delete exon 1 of PDGFB, and release this growth factor from its normal regulation.