Correspondence:

The online version of this article has a Supplementary Appendix. Background Aberrant activation of tyrosine kinases, caused by either mutation or gene fusion, is of major importance for the development of many hematologic malignancies, particularly myeloprolif-erative neoplasms. We hypothesized that hitherto unrecognized, cytogenetically cryptic tyro-sine kinase fusions may be common in non-classical or atypical myeloproliferative neoplasms and related myelodysplastic/myeloproliferative neoplasms. Design and Methods To detect genomic copy number changes associated with such fusions, we performed a sys-tematic search in 68 patients using custom designed, targeted, high-resolution array compara-tive genomic hybridization. Arrays contained 44,000 oligonucleotide probes that targeted 500 genes including all 90 tyrosine kinases plus downstream tyrosine kinase signaling components, other translocation targets, transcription factors, and other factors known to be important for myelopoiesis