Tanizawa RS, Azevedo Neto RS, Kumeda CA, Leal AM, Ferreira PB, Velloso ED Figure 5 – Kaplan-Meier survival curves according to the cytogenetic profile, normal vs. abnormal and with complex karyotypes (p-value = 0.123). Binary logistic regression analysis for overall survival-related factors showed that the presence of an abnormal karyotype was an independent factor for reduced survival (p-value = 0.012). Discussion The results obtained from our sample are concordant with those of other authors, reinforcing the importance of cytogenetics, both in the diagnosis and prognosis of secondary MN. The high rate of clonal abnormalities (84.4%) observed here is similar to other studies that reported karyotype abnormalities in 80-95% of patients with secondary MN.(6) Also, the predominance of unbalanced abnormalities (96.3%), the high frequency of complex karyotypes (44.4%) and chromosome 7 monosomy (37%) are consistent with the literature.(6,7,9) In particular, monosomy 7 was described in patients following AA; this cytogenetic abnormality has been reported to be recurrent in secondary MN of patients with medullar failure treated with immunosuppressants and G-CSF.(8,17,22) Curiously, the only case of balanced abnormality with t(3;21) was a patient (Patient 9) who had been treated for multiple myeloma using an alkylating agent (melphalan). Balanced abnormalities involving the CBFB (16q22), RARA (17q21) and AML1 (21q22) genes have been reported more frequently after the use of topoisomerase inhibitors. The presence of the t(3;21)(q26;q22) translocation that leads to the fusion of the EVI1(3q26) and AML1 or RUNX1 (21q22) genes has been frequently reported in MN-t and in the blast crisis stage of CML.(23) In the present sample, no rearrangements of the 11q23 region were observed; the importance of investigating the integrity of the MLL gene by FISH must be remembered, given the fact that the MLL rearrangement may remain cryptic by conventional cytogenetic methods.(24) Cytogenetic abnormalities are known to be independent prognostic factors in de novo MDS and are incorporated in the most commonly used prognostic scores such as the 430 International Prognostic Scoring System (IPSS) and WHO Prognostic Scoring System (WPSS).(25,26) Yet in secondary MN, the prognostic factors are less well studied, with variables such as age, primary disease, platelet count, hemoglobin concentration, serum protein and C-reactive protein levels, cytogenetic analysis, medullar fibrosis and CD34 cell expression in bone marrow histology, all being associated with survival.(27-30) The prognosis of MN-t is highly reserved, with a median survival time estimated at 6 months; the cytogenetic study plays an important role, not only for prognosis, but in the follow-up after HSCT.(7,12) In this study, abnormal karyotype proved to be an independent factor for poorer survival (p-value = 0.03), while complex karyotype alterations showed a slight tendency towards a reduced survival (p-value = 0.057) compared to the other cytogenetic abnormalities. Secondary MNs are becoming more common; this is the price of longer survival of patients with neoplasias. The treatment of chronic lymphoproliferative diseases with purine analogs associated with alkylating agents, as well as high-intensity therapeutic regimens, followed by autologous transplantation are current examples of this scenario. Moreover, in the field of non-neoplastic hematological diseases, a clear increase in the incidence of MDS is observed in patients with AA. Despite the unfavorable prognosis of secondary MNs, karyotype analysis allows the stratification of these patients. New drugs, such as hypomethylating agents, are the subject of research as a "bridge" until a suitable donor for allogeneic HSCT can be found. References 1. Luna-Fineman S, ShannonKM, Lange BJ. Childhood monosomy 7: Epidemiology, biology, and mechanistic implications. Blood. 1995;85(8):1985-99. 2. Huebner G, Karthaus M, Pethig K, Freund M, Ganser A. Myelodysplastic syndrome and acute myelogenous leukemia secondary to heart transplantation. Transplantation. 2000;70(4): 688-90. 3. Naschitz JE. Rheumatic syndromes: clues to occult neoplasia. Curr Opin Rheumatol. 2001;13(1):62-6. 4. Jesus G, Barcelos A, Neves C, Crespo J. Manifestações reumáticas e neoplasias. Acta Reum Port. 2006;31(4):305-21. 5. Vardiman JW, Arber DA, Brunning RD, Larson RA, Matiutes E, Baumann I, et al. Therapy-related myeloid neoplasms. In: Swerdlow SH, Campo E, Harris NL, Jafe ES, Pileri SA, Stein H, et al., editors. WHO Classification of Tumours of Haematopoietic and Lymphoid Tissues. Lyon: IARC Press; 2008. p.127-9. 6. Heim S. Cytogenetics findings in primary and secondary MDS. Leuk Res.1992;16(1):43-6. 7. Kröger N, Brand R, van Biezen A, Zander A, Dierlamm J, Niederwieser D, Devergie A, Ruutu T, Cornish J, Ljungman P, Gratwohl A, Cordonnier C, Beelen D, Deconinck E, Symeonidis A, de Witte T; Myelodysplastic Syndromes Subcommittee of The Chronic Leukaemia Working Party of European Group for Blood and Marrow Transplantation (EBMT). Risk factors for therapy-related myelodysplastic syndrome and acute myeloid leukemia treated with allogeneic stem cell transplantation. Haematologica. 2009; 94(4):542-9. Comment in: Haematologica. 2009;94(4):454-9. Rev Bras Hematol Hemoter. 2011;33(6):425-31