Amsterdam, The Netherlands, June 13-16, 2019 A. Paiva4,7, A. Pereira4,8, J. Azevedo6, M. L. Ribeiro4,6, J. Barbosa de Melo2,4,5, A. Gonçalves3,4,5, I. M. Carreira2,4,5, A. B. Sarmento-Ribeiro3,4,5,6,* 1 Clinical Hematology Department, 2Laboratory of Cytogenetics and Genomics, Laboratory of Oncobiology and Hematology and University Clinic of Hematology, 4 Coimbra Institute for Clinical and Biomedical Research (iCBR) - Group of Environment Genetics and Oncobiology (CIMAGO), Faculty of Medicine, University of Coimbra (FMUC), 5Center for Innovative Biomedicine and Biotechnology (CIBB), University of Coimbra, 6Clinical Hematology Department, 7Flow Cytometry Unit, Clinical Pathology Service, Centro Hospitalar Universitário de Coimbra (CHUC), Coimbra, 8Medicine Department, Hospital Distrital da Figueira da Foz, Figueira da Foz, Portugal 3 Downloaded from http://journals.lww.com/hemasphere by BhDMf5ePHKbH4TTImqenVCEuRsfpwK1FkjwELjO164UaFxkWGlu3Qpxzb5iFeSWZF6y+Qdt5VQY= on 12/08/2019 Background: Genomic abnormalities play a key role in the biological properties and clinical behavior of hematological malignancies, namely in chronic lymphocytic leukemia (CLL) and multiple myeloma (MM). These diseases have particularly benefited from gene expression profiling and genomic characterization, which improved diagnosis, prognosis and therapy response prediction. Conventional cytogenetics (CC) and fluorescence in situ hybridization (FISH) play a crucial role in the detection of cytogenetics abnormalities in these hematologic malignancies. However, these techniques had limitations, while CC requires proliferating cells and FISH is a targeted technique, underestimating the extent of chromosomal changes. Array comparative genomic hybridization (aCGH) had facilitated diagnosis and gene discovery with the ability to perform genome-wide research and in high concordance with the cytogenetic and FISH results. These features facilitate the detection of clinically relevant findings that would be missed by other techniques. Aims: Therefore, the aim of this study was to screen and identify new genomic events in CLL and MM patients by aCGH in order to identify new potential prognostic biomarkers. Methods: To this end, 19 CLL patients at diagnosis [9 females/10 males; 74 years (50–90); Binet stage (n = 18): A (n = 15, 83%) e C (n = 3, 17%)], 1 monoclonal B lymphocytosis (MBL; male; 81 years) and 10 MM patients (4 females/6 males; 74 years (54–90) were analyzed by aCGH. Genomic DNA was obtained from peripheral blood mononuclear cells of CLL patients and from plasma cells (CD138+ isolated by MACS) from bone marrow samples of MM patients. The results were analyzed statistically considering a significance level of 95% (p < 0.05). Results: Results show that CLL patients have a median of 8 copy number variants (CNVs) per patient, ranging from 3 to 11, and MM patients have a median of 10 CNVs/patient, ranging from 1 to 23. Among the 137 CNVs detected in CLL patients, 65% were losses (n = 87) and 35% gains (n = 47), with an average of 4.4 losses/CLL case and 2.4 gains/CLL case. The patient with MBL had 10 CNVs (4 losses and 6 gains). In MM patients were detected 107 CNVs, 37% were losses (n = 40) and 63% gains (n = 67) with an average of 4.0 losses/MM case and 6.7 gains/MM case. These CNVs have several sizes ranging from 50 bp to 130 Mb in CLL and from 8.6 Kb to 131 Mb in MM, encompassing genes with malignant potential. We found several recurrent CNVs in CLL patients: 7 del(14q) (35%); 7 del(13q) (35%), 6 tris 12 (30%), 2 del(11q) (10%), 5 del(6q) (25%), 3 del(8p) (15%), 2 dup(8q) (10%) and 2 dup(2p) (5%). We also found 2 del(9p21.3) (10.0%), a rare abnormality in CLL. Additionally, all high-risk patients (Binet C) have a del(14q) but these CNVs were less frequent in low-risk CLL patients (Binet A: 20%, n = 3, p = 0,007). In MM patients the following recurrent CNVs were found: 7 del(13q) (70%), 5 dup(1q) (50%), 4 tris 9 (40%) and 4 del(14q) (40%). Events involving X chromosome, including monosomy and trisomy, were detected in 4 MM patients (40%). Interestingly, 6 out of 7 patients with del(13q) present a minimal deleted region (13q14.11-q14.3) established previously by other groups. Summary/Conclusion: This study suggests that MM patients have a higher genomic complexity than CLL patients and that aCGH have potential to identify new prognostic markers in these pathologies. PB1886 THE TRANSMEMBRANE RECEPTOR TYROSINE KINASE-LIKE ORPHAN RECEPTOR 1 IN CHRONIC LYMPHOCYTIC LEUKEMIA A. Senturk Yikilmaz1,*, D. N. Avcı2, S. Mine Bakanay1, S. Akinci2, M. Falay2, G. Ozet1, I. Dilek1 1 Hematology, Yıldırım Beyazıt University, 2Hematology, Bilkent City Hospital, Ankara, Turkey Background: B-cell chronic lymphocytic leukemia (CLL) is the most common haematological malignancy in advanced age. The clinical course of the disease is highly variable, therefore there is a need to investigate the various prognostic factors. The transmembrane receptor tyrosine kinase-like orphan receptor 1 (ROR1) is upragulated in chronic lymphocytic leukemia | 2019;3:S1 (CLL) cells. ROR1 has a special expression on CLL as a diagnostic marker. Aims: The aim of this study was to compare the relationship between expression of ROR on CLL cells and clinical / laboratory features of CLL patients. Methods: Between February 2010 and June 2018, 30 cases diagnosed with CLL were analyzed. CLL cases were divided into 2 different groups as high (HrROR1) or low (LrROR1) ROR1 expression according to flow cytometric analysis at initial diagnosis. Clinical and laboratory findings of 2 groups were compared during the mean follow-up period of 19 months. Statistical analyzes were performed using chi-square test using SPSS version 16.0 (SPSS Inc., Chicago, IL, USA). A value of less than 0.05 was considered significant. Receiver operating characteristic (ROC) curves were formulated to estimate a cut-off of ROR 1 for advanced stage disease. A two- sided p value <0,05 was considered statistically significant. Results: The clinical and laboratory data of 30 CLL patients with a median age of 60 (37–83) years and with Female/Male ratio of 16/14 were evaluated. Mean follow-up time was 38.5 (SD ± 34.1) months. One patient (3.3%) died during follow-up. The number of cases with RAI stage 0–1, stage 2, stage 3–4 was 14 (46.7%), 11 (36.6%) and 5 (16.7%). The CD 38 positivity of the patients was 10% with flow cytometry analysis. ROC were used to obtain cutoff levels of ROR1 positivity for RAI stage (early versus intermediate+high). We established a cut-off level of 60% for ROR1 percentage in these subjects for intermediate + high RAI stage (p: 0.032). The calculated cut-off levels had the highest sensitivity compared to the other cut-off levels. The ROC area for percentage of ROR1 was 0,73 with a cutoff value of 60% of ROR1 positivity. The sensitivity and specificity was 92.9% and 62.5%, respectively (figure 1). The count of high rate of ROR1(HrROR1) positivity patients were 20 (66.7%) cases. The clinical and laboratory findings of HrROR1 patients and LrROR1 positivity patients were compared each other (Shown in Table 3). HrROR 1 positivity was associated with presence of splenomegaly (p = 0.011), presence of anemia (p = 0.002) and high beta 2 microglobulin value ≥3 mg/dL and the need for first line treatment (p = 0.029). In 5 out of the 12 patients who had anemia at the initial diagnosis, anemia was related with involvement of CLL. When 7 patients whose anemia is not associated with CLL disease involvement were excluded, HrROR 1 positivity was still associated with the presence of anemia (p = 0.046). All patients in need of first line treatment were in the patient group with HrROR1 positivity. Summary/Conclusion: In our CLL patients, higher rate of ROR1(HrROR1) positivity is related to presence of splenomegaly, presence of anemia, beta 2 microglobulin value ≥3 mg/dL, having RAI Stage 2/3/4 disese and need for first line treatment. PB1887 THE SIGNIFICANCE OF CD43, CD81, CD200, AND ROR1 FOR DIFFERENTIAL DIAGNOSIS OF CLL AS MULTICOLOR FLOW CYTOMETRY M. Falay1,*, M. Serdar2, S. Dagdas1, S. Pepeler1, M. A. Ucar1, G. Ozet1 1 hematology, ankara numune education and resarch hospital, Ankara, 2Biochemistry, Acıbadem University Med. Faculty, Istanbul, Turkey 859