In this study, we describe a novel fusion in hematological malig- nancies, expanding number of FGFR1 partner genes and confirming the relevance of RANBP2/NUP358 in myeloid neoplasm. The clinical presentation as a myeloproliferative/myelodysplastic disorder was not different from other EMS. More cases with chromosome 2 abnormalities should be explored in order to evaluate the incidence of RANBP2/NUP358 rearrangements in hematological neoplasms. CONFLICT OF INTEREST The authors declare no conflict of interest. ACKNOWLEDGEMENTS We thank Dr Elisabeth FLORI for providing part of the BACs. C Gervais 1,2,3 , L Dano 1,2,3 , N Perrusson 4 , C He ´ lias 1,2,3 , E Jeandidier 2,3 , A-C Galoisy 1,3 , A Ittel 1,2,3 , R Herbrecht 5 , K Bilger 5 and L Mauvieux 1,2,3,4 1 Po ˆle de Biologie, Laboratoire d’He ´matologie, Ho ˆpitaux Universitaires de Strasbourg, Strasbourg, France; 2 Laboratoire Re ´gional de Cytoge ´ne ´tique He ´matologique d’Alsace Mulhouse–Strasbourg, Strasbourg, France; 3 Plateforme Re ´gionale INCa de Ge ´ne ´tique Mole ´culaire des Cancers d’Alsace, Strasbourg, France; 4 Laboratoire d’He ´matologie Cellulaire, Faculte ´ de Me ´decine de Strasbourg, Strasbourg, France and 5 De ´partement d’Onco-He ´matologie, Ho ˆpitaux Universitaires de Strasbourg, Strasbourg, France, E-mail: laurent.mauvieux@chru-strasbourg.fr REFERENCES 1 Swerdlow SH, Campo E, Harris NL, Jaffe ´ ES, Pileri SA, Stein H et al. WHO Classifi- cation of Tumours of Haematopoietic and lymphoid tissues. IARC: Lyon, 2008. 2 Li F, Zhai YP, Tang YM, Wang LP, Wan PJ. Identification of a novel partner gene, TPR, fused to FGFR1 in 8p11 myeloproliferative syndrome. Genes Chromosomes Cancer 2012; 51: 890–897. 3 Wasag B, Lierman E, Meeus P, Cools J, Vandenberghe P. The kinase inhibitor TKI258 is active against the novel CUX1-FGFR1 fusion detected in a patient with T-lymphoblastic leukemia/lymphoma and t(7;8)(q22;p11). Haematologica 2011; 96: 922–926. 4 Jackson CC, Medeiros LJ, Miranda RN. 8p11 myeloproliferative syndrome: a review. Hum Pathol 2010; 41: 461–476. 5 Shaffer LG, Slovak ML, Campbell LJ. An International System for Human Cytogenetic Nomenclature. Karger: Basel, 2009. 6 Ma Z, Hill DA, Collins MH, Morris SW, Sumegi J, Zhou M et al. Fusion of ALK to the Ran-binding protein 2 (RANBP2) gene in inflammatory myofibroblastic tumor. Genes Chromosomes Cancer 2003; 37: 98–105. 7 Hidalgo-Curtis C, Chase A, Drachenberg M, Roberts MW, Finkelstein JZ, Mould S et al. The t(1;9)(p34;q34) and t(8;12)(p11;q15) fuse pre-mRNA processing proteins SFPQ (PSF) and CPSF6 to ABL and FGFR1. Genes Chromosomes Cancer 2008; 47: 379–385. 8 Soler G, Nusbaum S, Varet B, Macintyre EA, Vekemans M, Romana SP et al. LRRFIP1, a new FGFR1 partner gene associated with 8p11 myeloproliferative syndrome. Leukemia 2009; 23: 1359–1361. 9 Wu J, Matunis MJ, Kraemer D, Blobel G, Coutavas E. Nup358, a cytoplasmically exposed nucleoporin with peptide repeats, Ran-GTP binding sites, zinc fingers, a cyclophilin A homologous domain, and a leucine-rich region. J Biol Chem 1995; 270: 14209–14213. 10 Bernad R, van der Velde H, Fornerod M, Pickersgill H. Nup358/RanBP2 attaches to the nuclear pore complex via association with Nup88 and Nup214/CAN and plays a supporting role in CRM1-mediated nuclear protein export. Mol Cell Biol 2004; 24: 2373–2384. 11 Patel AS, Murphy KM, Hawkins AL, Cohen JS, Long PP, Perlman EJ et al. RANBP2 and CLTC are involved in ALK rearrangements in inflammatory myofibroblastic tumors. Cancer Genet Cytogenet 2007; 176: 107–114. 12 Chen ST, Lee JC. An inflammatory myofibroblastic tumor in liver with ALK and RANBP2 gene rearrangement: combination of distinct morphologic, immunohistochemical, and genetic features. Hum Pathol 2008; 39: 1854–1858. 13 Rottgers S, Gombert M, Teigler-Schlegel A, Busch K, Gamerdinger U, Slany R et al. ALK fusion genes in children with atypical myeloproliferative leukemia. Leukemia 2010; 24: 1197–1200. 14 Aslanukov A, Bhowmick R, Guruju M, Oswald J, Raz D, Bush RA et al. RanBP2 modulates Cox11 and hexokinase I activities and haploinsufficiency of RanBP2 causes deficits in glucose metabolism. PLoS Genet 2006; 2: e177. 15 Graux C, Cools J, Melotte C, Quentmeier H, Ferrando A, Levine R et al. Fusion of NUP214 to ABL1 on amplified episomes in T-cell acute lymphoblastic leukemia. Nat Genet 2004; 36: 1084–1089. Supplementary Information accompanies the paper on the Leukemia website (http://www.nature.com/leu) Exome sequencing in tracking clonal evolution in multiple myeloma following therapy Leukemia (2013) 27, 1188–1191; doi:10.1038/leu.2012.287 Sequencing the tumor genome using next-generation sequencing (NGS) is providing an unparalleled insight into the pathogenesis and progression of the disease. Much of the current focus of NGS in cancer is on defining mutations in the tumor genome at disease presentation, and these findings are central to under- standing the molecular mechanisms that underlie pathogenesis. However, additional questions remain about the stability of the tumor clone under therapeutic pressure and these require a distinct second wave of NGS analyses. Understanding how each tumor evolves following therapy will be the key to delivering targeted therapy tailored for individual patients and in develop- ing stratified therapeutic programs. Where a given tumor presents as a highly heterogeneous disease, this introduces a further complexity, requiring each subset of the disease to be evaluated separately in its response to therapy. Multiple myeloma (MM), defined as accumulation of malignant plasma cells in the bone marrow, exemplifies such a tumor and exhibits marked disease heterogeneity at presentation. 1,2 At the outset, aberrant chromosomal markers exist in diagnostic MM samples that are associated with poor prognosis and help in delineating specific disease subsets, including t(4;14) and 1q21 amplification among others, 1–5 suggesting that these markers may be highly relevant to defining specific patterns of progression and clonal response to therapy. The pivotal NGS study of MM centered on the MM Research Consortium (MMRC) analysis of 38 tumor genomes that identified key somatic mutations, either at disease presentation or at relapse, but not in a paired setting. 6 Consequently, the data did not permit Accepted article preview online 9 October 2012; advance online publication, 13 November 2012 Letters to the Editor 1188 Leukemia (2013) 1172 – 1218 & 2013 Macmillan Publishers Limited