(2009) Donor cell-derived myelodysplastic syndrome after cord blood transplantation. Bone Marrow Transplantation, 43, 429–431. Kytta ¨la ¨, S., Habermann, I., Minami, T., Ehninger, G. & Kiani, A. (2009) Regulation of Down Syndrome Critical Region 1 expression by Nuclear Factor of activated T cells in megakaryocytes. British Journal of Haematology, 144, 395–408. Malinge, S., Izraeli, S. & Crispino, J.D. (2009) Insights into the man- ifestations, outcomes, and mechanisms of leukemogenesis in Down syndrome. Blood, 113, 2619–2628. O’Connell, R.M., Rao, D.S., Chaudhuri, A.A., Boldin, M.P., Taganov, K.D., Nicoll, J., Paquette, R.L. & Baltimore, D. (2008) Sustained expression of microRNA-155 in hematopoietic stem cells causes a myeloproliferative disorder. Journal of Experimental Medicine, 205, 585–594. Ruiz-Argu ¨elles, G.J., Ruiz-Argu ¨elles, A. & Garce ´s-Eisele, J. (2007) Donor cell leukaemia: a critical review. Leukaemia & Lymphoma, 48, 25–38. Salek-Ardakani, S., Smooha, G., de Boer, J., Sebire, N.J., Morrow, M., Rainis, L., Lee, S., Williams, O., Izraeli, S. & Brady, H.J. (2009) ERG is a megakaryocytic oncogene. Cancer Research, 69, 4665– 4673. Sevilla, J., Querol, S., Molines, A., Gonza ´lez-Vicent, M., Balas, A., Carrio ´ , A., Estella, J., Angel Dı ´az, M. & Madero, L. (2006) Transient donor cell derived myelodysplastic syndrome with monosomy 7 after unrelated cord blood transplantation. European Journal of Haematology, 77, 259–263. Keywords: donor cell-derived leukaemia, umbilical cord blood transplantation, oncogenic co-amplification, RUNX1, DSCR genes. First published online 25 August 2010 doi:10.1111/j.1365-2141.2010.08350.x Jumping translocations of the long arms of chromosome 1 in myeloid malignancies is associated with a high risk of transformation to acute myeloid leukaemia* Jumping translocations (JT) are rare cytogenetic phenome- non resulting from a part of one chromosome translocating to several recipient chromosomes, creating multiple related clones within a single patient. A detailed review of these abnormalities was recently published (Berger & Bernard, 2007). The occurrence of JT and, specifically, amplification of the long arms of chromosome 1 (1qJT) is an independent indicator of poor outcome in multiple myeloma patients (Sawyer et al, 2005; Hanamura et al, 2006) but due to their rarity in myeloid malignancies (Najfeld et al, 1995; Djordjevic et al, 2008; Manola et al, 2008) it is uncertain whether this abnormality contributes to disease progression. We retro- spectively investigated 1qJT in 23 patients with myeloprolif- erative neoplasm (MPN) and myelodysplastic syndrome (MDS) who were evaluated in the Tumor Cytogenetics Laboratory at the Mount Sinai School of Medicine between 1984 and 2009. Two of these patients (Patients 8 and 22) have been previously reported (Najfeld et al, 1995). Diagnoses were made according to the World Health Organization classification criteria. Tables I and S1 outline the characteristics of the 23 patients with 1qJT. Among 512 studied patients with MPN (poly- cythaemia vera [PV] = 361, primary myelofibrosis [PMF] = 151), 3 (PV = 2, PMF = 1) were identified who had 1qJT at diagnosis (0Æ6% incidence). Additionally four of 165 (PV = 96, PMF = 69) patients with MPN-acquired 1qJT over a period of 11 years (the overall incidence was 1Æ3% or 4Æ2% among cytogenetically abnormal). The mean follow up of the five patients was 65 months and the mean time from diagnosis to the development of 1qJT was 47 months. Four of these five patients transformed to acute myeloid leukaemia (AML) within 8 months of acquiring 1qJT. Patient 1 initially had a del(5q) alone for 3 years, and over the next 6 years developed a der(14)t(1;14)(q12;p11) subclone in three cells. A study performed 2 years later, at the time of transformation to AML, revealed five clonal populations with +1q translocated to chromosomes 4, 9, 14, 19, 21 and 22. Patient 5 initially had +1q and then developed two copies of der(9)t(1;9)(q21;q12) 38 months later (Fig. 1E). This obser- vation provides evidence that a recurrent der(9)t(1;9) abnor- mality originate from +1 with subsequent breakage within heterochromatin of 1q and reunion with the satellite III of chromosome 9 (Sambani et al, 2005). Patient 6 had i(9)(p10) but developed a der(6)t(1;6)(q21;q27) subclone in two of 18 cells after 6 years. Over time the subclone involved 100% of cells. The patient was treated solely with interferon. The most recent analysis revealed 1qJT to chromosomes 6, 7, Y as well as dup(1)(q21) (Fig. 1A–D). The initial cytogenetic analysis of 16 patients with MDS/ AML revealed a normal karyotype in 8 patients and an abnormal karyotype in the other eight patients. Out of 532 MDS patients studied between 1986 and 2009 we identified Correspondence 288 ª 2010 Blackwell Publishing Ltd, British Journal of Haematology, 151, 285–291