Abstract 5011: Difference in expression of STAT3 and STAT5b in Swedish and Egyptian patients with activated b-cell subtype of diffuse large b-cell lymphoma

Abstract

Abstract Diffuse Large B-cell lymphoma (DLBCL), the most common type of lymphoma in adults, accounts for approximately 30 to 40% of newly diagnosed lymphomas. Using gene expression profiling, DLBCL can be divided into three immunologically indistinguishable subtypes: the germinal center B-cell like (GBC), the activated B-cell like (ABC) and the primary mediastinal B-cell lymphoma (PMBL) subtype. The aim of the study was to compare gene expression profiles of Swedish and Egyptian ABC DLBCL patients. Formalin fixed and paraffin embedded material of 67 Egyptian and 15 Swedish ABC DLBCL patients were used in the study. Affymetrix gene expression platform was used for profiling and the analysis was carried out using GeneSpring GX software. Quantitative PCR (qPCR) and confocal microscopy was used to verify the findings. The GeneSpring GX analysis showed that 3247 genes were at least 2 fold up- or downregulated comparing the two patient groups. Among these were 1827 genes upregulated and 1420 genes downregulated. Gene expression analysis was verified using qPCR showing that STAT3 was upregulated with a fold change of 3.1 in the Swedish patients and that STAT5b was upregulated with a fold change of 1.3 in the Egyptian patients. Confocal microscopy showed protein activity of STAT3 and 5b in the nucleus of Swedish and Egyptian patients respectively using monoclonal antibodies. This is the first study that reveals diversity in expression of STATs in different populations of ABC DLBCL patients. STAT3 and 5b are known to have different pathways of activation and targeted disruption has shown their functional differences. Using gene expression profiling, we revealed different expression levels of STAT3 and STAT5b in Swedish and Egyptian ABC DLBCL patients. Since the populations of Sweden and Egypt are exposed to different infectious agents, the results of the present study further raise the question concerning viral etiology in ABC-DLBCL possibly due to repeated infections and chronic inflammation. In general, these findings give additional evidence to the importance of signaling pathways involving STATs in ABC DLBCL. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 5011. doi:10.1158/1538-7445.AM2011-5011