According to the 2016 World Health Organization classification, myeloid neoplasms with eosinophilia (MPN-Eo) are associated with genetic abnormalities of genes coding for type III tyrosine kinase (TK) receptors, mainly PDGFRA, PDGFRB and FGFR1, but also JAK2. 1 Beside these translocations, very rare FLT3 gene rearrangements have been reported, which raises the double question of its association with myeloid neoplasms and of its specific targeted therapy. 2-7

A new t (3; 13)(q13; q12) was found from a case of atypical mixed lymphoid/myeloid neoplasm. This case, diagnosed MPN-Eo, was characterized by the coexistence of bone marrow myeloproliferation with circulating hypereosinophilia and T-cell lymphoblastic lymphoma in lymph node (Supplementary Results for detailed description). The patient could not benefit from new tyrosine kinase inhibitors. Evolution was fatal in 3 months despite conventional CHOP chemotherapy (Cyclophosphamide, Hydroxydaunorubicin, Oncovin and Prednisolone). Karyotype of tumor cells from lymph nodes and bone marrow revealed a single clonal t (3; 13)(q13; q12) translocation (Figure 1a, left panel). Absence of FGFR1 gene rearrangement was checked by fluorescence in situ hybridization (FISH) and RT-PCR according to methods described by others. 8 BCR-ABL gene translocation, FLT3-ITD and D835 mutation were also absent. FISH walking on both chromosomes 3 and 13 with BAC and fosmid probes showed that the breakpoint was located in a 58.6 kb region encompassing HCLS1 and GOLGB1 on chromosome 3 and in a 65.5 kb region containing the FLT3 locus on chromosome 13 (Figure 1a, right panel).