Aurora-B expression may not contribute to disease progression: a reflection of the heterogeneous pathogenesis?

We read with great interest the paper by Yoshida et al. entitled " Marked upregulation of survivin and Aurora-B kinase are associated with disease progression in the myelodysplastic syndromes ". 1 Aurora kinases are key players in ensuring accurate chromosome segregation during the cell cycle, maintaining genetic integrity in cell division. 2 Over the last few years, much attention has been focused on the involvement of these proteins in the process of tumorigenesis. High Aurora-B and Aurora-A expression has been reported in various types of commonly occurring malignancy and, in some cases, correlated with aneuploidy and poor prognosis. Despite the many reports of high expression of Aurora-B and Aurora-A in solid tumors, 3,4 information regarding expression in hematologic malignancies is still limited, 5,6,7 especially in MDS. Our study included 61 MDS patients, 31 male and 30 female (median age 66 years; range 15-91 years). According to WHO classification, there were 6 patients with refractory anemia (RA), 2 patients with refractory neutropenia (RN), 2 patients with isolated del(5q), 9 patients with ring sideroblasts (RARS), 28 patients with refractory cytopenia with multilineage dysplasia (RCMD), 3 patients with RA with excess of blasts 1 (RAEB-1), 5 patients with RA with excess of blasts 2 (RAEB-2), and 6 patients with therapy-related MDS. Four samples from healthy volunteers were used as controls. Among these patients, 85% were stratified as low risk and 15% as high risk according to IPSS. Total RNA from MDS patients and donor bone marrow cells were isolated using Trizol reagent (Invitrogen, Carlsbad, CA, USA). To analyze aurora kinases genes, TaqMan Assays were used (Aurora-A: Hs00269212_m1 and Aurora-B: Hs00177782_m1; Applied Biosystems). β2-microglobulin (B2M: Hs99999907_m1) and Ubiquitin C (UBC: Hs00824723_m1) were chosen as endogeneous internal control for each sample. The comparative cycle threshold (Ct) method was used to determine the relative expression levels of Aurora-B and Aurora-A genes. Their haematologica 2012; 97:e37 LETTERS TO THE EDITOR Table 1. Age, sex, WHO and IPSS classification, karyotype and gene expression of 61 MDS patients.