pain. Hussein et al. 8 state that repair of three to four vertebrae per augmentation is reasonable. We also reported up to 16 repairs in one patient in the same paper (Figure 1e). While the majority (75%) of the 792 patients in this study required a single vertebral augmentation session, the median number of repairs was consistent with other studies at two per session. Augmentation repairs have been noted in levels up to the cervical area, and percutaneous repairs in the T3-L5 levels are considered safe and effective. 5,8 Others have differed in size requirements to successfully augment vertebral collapse and placed upper limits from T7 to T3. 10,11 However, repairs in our study were successfully made at the upper T1-T5 thoracic levels (4.7%). Subsequent to this study, we have successfully included some cervical levels. Limitations of our study include not assessing the potentially confounding effects of multiple myeloma therapy (for example, steroids) on outcomes, observational design, and participation and recall bias. Outcomes assessment was complicated by cancer therapy and/or relocation, and mortality, which was not assessed in this study, cannot be ruled out as a reason for nonresponse in some cases. This report comprises the largest study of distribution of compression fractures in consecutive multiple myeloma patients and prospectively acquired outcomes in patients undergoing vertebral augmentation to date.

Cytogenetic aberrations identified by metaphase cytogenetics (MC) have diagnostic, prognostic, and therapeutic implications in myelodysplastic syndromes (MDS). However, in some MDS patients MC study is unsuccesful. Single nucleotide polymorphism array (SNP-A) based karyotyping could be helpful in these cases. We performed SNP-A in 62 samples from bone marrow or peripheral blood of primary MDS with an unsuccessful MC study. SNP-A analysis enabled the detection of aberrations in 31 (50%) patients. We used the copy number alteration information to apply the International Prognostic Scoring System (IPSS) and we observed differences in survival between the low/intermediate-1 and intermediate-2/high risk patients. We also saw differences in survival between very low/low/intermediate and the high/very high patients when we applied the revised IPSS (IPSS-R). In conclusion, SNP-A can be used successfully in PB samples and the identification of CNA by SNP-A improve the diagnostic and prognostic evaluation of this group of MDS patients.

Identifying additional genetic alterations associated with poor prognosis in acute lymphoblastic leukemia (ALL) is still a challenge. Aims: To characterize the presence of additional DNA copy number alterations (CNAs) in children and adults with ALL by whole-genome oligonucleotide array (aCGH) analysis, and to identify their associations with clinical features and outcome. Array-CGH was carried out in 265 newly diagnosed ALLs (142 children and 123 adults). The NimbleGen CGH 12x135K array (Roche) was used to analyze genetic gains and losses. CNAs were analyzed with GISTIC and aCGHweb software. Clinical and biological variables were analyzed. Three of the patients showed chromothripsis (cth6, cth14q and cth15q). CNAs were associated with age, phenotype, genetic subtype and overall survival (OS). In the whole cohort of children, the losses on 14q32.33 (p = 0.019) and 15q13.2 (p = 0.04) were related to shorter OS. In the group of children without good- or poor-risk cytogenetics, the gain on 1p36.11 was a prognostic marker independently associated with shorter OS. In adults, the gains on 19q13.2 (p = 0.001) and Xp21.1 (p = 0.029), and the loss of 17p (p = 0.014) were independent markers of poor prognosis with respect to OS. In summary, CNAs are frequent in ALL and are associated with clinical parameters and survival. Genome-wide DNA copy number analysis allows the identification of genetic markers that predict clinical outcome, suggesting that detection of these genetic lesions will be useful in the management of patients newly diagnosed with ALL.