Fusion of PCM1 to FGFR1 as the genetic driver for this myeloid neoplasm with eosinophilia. (A) Illustration of the in-frame fusion of PCM1 (exons 1-36) to FGFR1 (exons 11-18), resulting in amino acid 1947 of PCM1 juxtaposed to amino acid 429 of FGFR1. The coiled-coil motifs (blue, shown with corresponding amino acid numbers) of PCM1 are thought to drive dimerization of the FGFR1 tyrosine kinase domain (red, shown with corresponding amino acid numbers). (B) Partial GTG banded karyotype demonstrating both chromosomes 8. The normal chromosome (left) and the abnormal chromosome with a distinctly abnormal 8p region pattern caused by inv(8)(p11.2p22) (right). (C) Corresponding partial metaphase FISH karyotype using a home-brew break-apart FGFR1 probe set. A distinct gap between the 5′ FGFR1 centromeric (green) probe and the 3′ FGFR1 telomeric (red) probe is clearly observed on the abnormal chromosome 8 (right), consistent with paracentric inversion between the 8p11 and 8p22 bands.