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The JAK2 V617F activating tyrosine kinase mutation is an infrequent event in both \"atypical\" myeloproliferative disorders and myelodysplastic syndromes. Blood 106: 1207-1209, 2005.","DOI":"10.1182\/blood-2005-03-1183"},{"key":"10","unstructured":"10. Mc Lornan DP, Percy MJ, Jones AV, et al. Chronic neutrophilic leukemia with an associated V617F JAK2 tyrosine kinase mutation. Haematologica 90: 1696-1697, 2005."},{"key":"11","doi-asserted-by":"crossref","unstructured":"11. Lea NC, Lim Z, Westwood NB, et al. Presence of JAK2 V617F tyrosine kinase mutation as a myeloid-lineage-specific mutation in chronic neutrophilic leukaemia. Leukemia 20: 1324-1326, 2006.","DOI":"10.1038\/sj.leu.2404240"},{"key":"12","doi-asserted-by":"crossref","unstructured":"12. Kako S, Kanda Y, Sato T, et al. Early relapse of JAK2 V617F-positive chronic neutrophilic leukemia with central nervous system infiltration after unrelated bone marrow transplantation. Am J Hematol 82: 386-390, 2007.","DOI":"10.1002\/ajh.20805"},{"key":"13","doi-asserted-by":"crossref","unstructured":"13. Zhang X, Pan J, Guo J. Presence of the JAK2 V617F mutation in patient with chronic neutrophilic leukemia and effective response tointerferon &alpha;-2b. Acta Haematol 130: 44-46, 2013.","DOI":"10.1159\/000345851"},{"key":"14","doi-asserted-by":"crossref","unstructured":"14. Said SM, Leung N, Sethi S, et al. Myeloproliferative neoplasms cause glomerulopathy. Kidney Int 80: 753-759, 2011.","DOI":"10.1038\/ki.2011.147"},{"key":"15","unstructured":"15. Haas M, VanBeek C. Glomerular diseases associated with hematopoietic neoplasms: an expanding spectrum. Kidney Int 80: 701-703, 2011."},{"key":"16","unstructured":"16. Audard V, Larousserie F, Grimbert P, et al. Minimal change nephrotic syndrome and classical Hodgkin's lymphoma: report of 21 cases and review of the literature. Kidney Int 69: 2251-2260, 2006."},{"key":"17","doi-asserted-by":"crossref","unstructured":"17. Aggarwal N, Batwara R, McCarthy ET, et al. Serum permeability activity in steroid-resistant minimal change nephrotic syndrome is abolished by treatment of Hodgkin disease. Am J Kidney Dis 50: 826-829, 2007.","DOI":"10.1053\/j.ajkd.2007.06.021"},{"key":"18","unstructured":"18. Velosa JA, Holley KE, Torres VE, et al. Significance of proteinuria on the outcome of renal function in patients with focal segmental glomerulosclerosis. Mayo Clin Proc 58: 568-577, 1983."},{"key":"19","doi-asserted-by":"crossref","unstructured":"19. Dingli D, Larson DR, Plevak MF, et al. Focal and segmental glomerulosclerosis and plasma cell proliferative disorders. Am J Kidney Dis 46: 278-282, 2005.","DOI":"10.1053\/j.ajkd.2005.05.004"},{"key":"20","doi-asserted-by":"crossref","unstructured":"20. Doussis-Anagnostopoulou IA, Talks KL, Turley H, et al. Vascular endothelial growth factor (VEGF) is expressed by neoplastic Hodgkin-Reed-Sternberg cells in Hodgkin's disease. 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