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2968 Introduction: Increased bone marrow angiogenesis is a characteristic feature of multiple myeloma (MM). New blood vessels formation is provided by recruiting vascular endothelial cells from existing capillaries or circulating endothelial progenitor cells (EPC). EPCs have distinct monocytic features and can be cultured from CD14+ cells. In addition, monocytes were shown to contribute to angiogenesis as EPCs in vivo. It has been established that myeloid progenitor cells participate in the development of endothelial precursors. In MM, it has been reported that circulating EPCs carried the same chromosomal aberrations as neoplastic plasma cells (PC). It is possible that EPCs originate from common precursor that gives rise to both PCs and endothelial cells. The purpose of our pilot study was to clarify whether myeloid cells, CD14+ monocytes (CD14+MO), in MM might carry the same chromosomal abnormalities as CD138+PC. Methods: Total of 15 MM patients were enrolled in this pilot study; 93 % (14/15) typical MM; 7 % (1/15) plasma cell leukemia (PCL). CD138+PCs were isolated by magnetic-activated cell separation (MACS) from bone marrow mononuclear cells (BMMNC). CD14+MOs were isolated by fluorescence-activated cell sorting (FACS) from BMMNC after isolation of CD138+PCs. The purity of both cell populations was > 90%. Distinct BM cell fractions were analyzed for del(13q14), del(17p53), IgH gene rearrangement, hyperdiploidy and trisomy of chromosomes 5, 9, 15 by interphase fluorescence in situ hybridization (FISH) according to standard protocol. The cut-off level for detection of choromosomal aberarations was set to 20%. Results: FISH analysis proved at least one of studied chromosomal abnormalities in 20% (3/15) of MM patients (See Table 1; No.1 – No.3). In case No.1, a patient with PCL, CD14+MOs were positive for del(13q14)(31%), IgH gene rearrangement (46%) and trisomy 9 (47%). The same aberrations were found in CD138+PCs but with higher frequency (Table 1). Patient No.2 was positive for del(13q14)(35%) and for del(17p53)(39%) in CD14+MO but in CD138+PCs, the patient was positive further for hyperdiploidy (53%) and trisomy 5 (28%), 9 (56%) and 15 (60%). CD14+MOs of patient No.3 were positive only for trisomy 15 (25%) which corresponded to trisomy 15 (24%) in CD138+PCs. Other chromosomal abnormalities found in CD138+PCs of No.3 were not detected in CD14+MOs. Chromosomal aberrations identified in CD14+MOs of No.4 – No.15 did not reach the cut-off level for positivity (Table 1). Conclusion: In our pilot study, we demonstrated for the first time that bone marrow CD14+ monocytes of MM patients carried the same chromosomal aberrations as CD138+ plasma cells. The possible explanation is that CD14+MOs and CD138+PCs may origin from a common precursor. We hypothesize that myeloid cells might play a role in blood vessel formation as endothelial precursors and might be important in pathogenesis of multiple myeloma. It requires further study to elucidate the relationship between two distinct bone marrow populations and a potential role of CD14+cells in disease severity. Supported with research program MSM of Czech republic Nr. 0021622434 and LC06027. Disclosures: No relevant conflicts of interest to declare.

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2820 Poster Board II-796 The presence of chromosomal abnormalities detected by FISH in plasma cells is considered to be an important prognostic factor for patients with multiple myeloma. In this study we analysed the impact of gain(1)(q21), del(13)(q14), del(17)(p13), t(4;14) and (non)hyperdiploidy on prognosis in MM patients. Taking together 194 MM patients (median age 66 years) were successfully examined by FISH for presence of above named chromosomal abnormalities in plasma cells. A total of 47 patients (median follow-up 43.2 months; 91% first line treatment, 9% second line treatment) were treated by peripheral blood stem cells transplantation (PBSCT). A total of 86 patients (median follow-up 38.4 months; 38% first line treatment, 43% second line treatment, 19% >2 previous treatment lines) were treated by thalidomide based regimen (86% together with glucocorticoids and alkylating agens). A total of 61 patients (median follow-up 46.5 months; 16% first line treatment, 36% second line treatment, 33% third line treatment, 15% >3 previous treatment lines) were treated by bortezomib based regimen (53% with glucocorticoids and alkylating agens, 20% with glucocorticoids + anthracycline). Gain(1)(q21) was found in 52% (101/194), del(13)(q14) in 55% (69/125), del(17)(p13) in 12% (13/112), t(4;14) in 20% (18/90) and 44% (56/126) of cases were hyperdiploid. In any of the three treatment based groups of patients we haven't found any significant difference in TTP, OS and treatment response (ORR) between any studied positive/negative chromosomal abnormality except gain(1)(q21). See Table 1 for results overview (TTP only). In patients treated by PBSCT (regardless of their pre-treatment) significant difference in TTP and OS for positive/negative patients was observed (15.6 vs. 27.3 months, p=0.002 for TTP; 47.2 vs. NR months, p=0.001 for OS). Furthermore, we entirely focused on newly diagnosed patients divided them into three subgroups: (1) patients treated by PBSCT in first line (n=42), (2) patients treated by thalidomide based regimen in first line (n=33) and (3) patients treated by bortezomib based regimen in first line (n=10). We confirmed unfavourable impact of gain(1)(q21) in patients treated with PBSCT whereas TTP and OS in gain(1)(q21) positive/negative patients was 15.6 vs. 27.3 months, p=0.003 (TTP); 47.2 vs. 66.9 months, p=0.002 (OS). This difference in TTP/OS among gain(1)(q21) positive/negative patients was observed neither in thalidomide based subgroup [NR vs. 11.7 months, p=0.956 (TTP); NR vs. 34.4 months, p=0.683 (OS)] nor in bortezomib based subgroup [(8.5 vs. 6.5 months, p=0.549 (TTP); NR vs. 6.8, p=0.254 (OS)]. See Table 2 for results overview (TTP only). In this study we revealed gain(1)(q21) almost in one half of MM cases, and we defined the newly diagnosed MM patients carrying gain(1)(q21) as a unique group of patients with poor prognosis. Nevertheless, treatment based on bortezomib / thalidomide combination probably suppresses unfavourable prognostic impact of all studied chromosomal abnormalities including gain(1)(q21). This study was supported by grant LC06027 of Masaryk University, Brno, Czech Republic, and by grants MSM0021622415 and MSM0021622434 of Ministry of Education, Czech Republic, and by IGA grants NR/9317-3 and NS/10207-3/2009 of Ministry of Medicine, Czech Republic. Disclosures: No relevant conflicts of interest to declare.