Researcher: Kılıç, Emel Şen
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Kılıç, Emel Şen
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Publication Metadata only Topological, functional, and structural analyses of protein-protein Interaction networks of breast cancer lung and brain metastases(Ieee, 2017) N/A; N/A; Department of Computer Engineering; N/A; Department of Chemical and Biological Engineering; Halakou, Farideh; Gürsoy, Attila; Kılıç, Emel Şen; Keskin, Özlem; PhD Student; Faculty Member; Master Student; Faculty Member; Department of Computer Engineering; Department of Chemical and Biological Engineering; Graduate School of Sciences and Engineering; College of Engineering; Graduate School of Sciences and Engineering; College of Engineering; N/A; 8745; N/A; 26605Breast cancer is the second most common cause of death among women. However, it is not deadly if the cancerous cells remain in the breast. The life threat starts when cancerous cells travel to other parts of body like lung, liver, bone and brain. So, most breast cancer deaths derive from metastasis to other organs. In this study, we introduce novel proteins and cellular pathways that play important roles in brain and lung metastases of breast cancer using Protein-Protein Interaction (PPI) networks. Our topological analysis identified genes such as RPL5, MMP2 and DPP4 which are already known to be associated with lung or brain metastasis. Additionally, we found four and nine novel candidate genes that are specific to lung and brain metastases, respectively. The functional enrichment analysis showed that KEGG pathways associated with the immune system and infectious diseases, particularly the chemokine signaling pathway, are important for lung metastasis. On the other hand, pathways related to genetic information processing were more involved in brain metastasis. By enriching the traditional PPI network with protein structural data, we show the effects of mutations on specific protein-protein interactions. By using the different conformations of protein CXCL12, we show the effect of H25R mutation on CXCL12 dimerization.Publication Metadata only Topological, functional, and structural analyses of protein-protein interaction networks of breast cancer lung and brain metastases(Institute of Electrical and Electronics Engineers (IEEE), 2017) N/A; N/A; Department of Computer Engineering; N/A; Department of Chemical and Biological Engineering; Halakou, Farideh; Gürsoy, Attila; Kılıç, Emel Şen; Keskin, Özlem; PhD Student; Faculty Member; Master Student; Faculty Member; Department of Computer Engineering; Department of Chemical and Biological Engineering; Graduate School of Sciences and Engineering; College of Engineering; Graduate School of Sciences and Engineering; College of Engineering; N/A; 8745; N/A; 26605Breast cancer is the second most common cause of death among women. However, it is not deadly if the cancerous cells remain in the breast. The life threat starts when cancerous cells travel to other parts of body like lung, liver, bone and brain. So, most breast cancer deaths derive from metastasis to other organs. In this study, we introduce novel proteins and cellular pathways that play important roles in brain and lung metastases of breast cancer using Protein-Protein Interaction (PPI) networks. Our topological analysis identified genes such as RPL5, MMP2 and DPP4 which are already known to be associated with lung or brain metastasis. Additionally, we found four and nine novel candidate genes that are specific to lung and brain metastases, respectively. The functional enrichment analysis showed that KEGG pathways associated with the immune system and infectious diseases, particularly the chemokine signaling pathway, are important for lung metastasis. On the other hand, pathways related to genetic information processing were more involved in brain metastasis. By enriching the traditional PPI network with protein structural data, we show the effects of mutations on specific protein-protein interactions. By using the different conformations of protein CXCL12, we show the effect of H25R mutation on CXCL12 dimerization.Publication Open Access Activating mutations of STAT5B and STAT3 in lymphomas derived from ??-T or NK cells.(Nature Publishing Group (NPG), 2015) Kucuk, Can; Jiang, Bei; Hu, Xiaozhou; Zhang, Wenyan; Chan, John K. C.; Xiao, Wenming; Alkan, Can; Williams, John C.; Avery, Kendra N.; Kavak, Pinar; Scuto, Anna; Gaulard, Philippe; Staudt, Lou; Iqbal, Javeed; Zhang, Weiwei; Cornish, Adam; Gong, Qiang; Yang, Qunpei; Sun, Hong; d'Amore, Francesco; Leppa, Sirpa; Liu, Weiping; Fu, Kai; de Leval, Laurence; McKeithan, Timothy; Chan, Wing C.; N/A; Department of Chemical and Biological Engineering; Lack, Nathan Alan; Kılıç, Emel Şen; Faculty Member; Department of Chemical and Biological Engineering; School of Medicine; Graduate School of Sciences and Engineering; 120842; N/ALymphomas arising from NK or gamma delta-T cells are very aggressive diseases and little is known regarding their pathogenesis. Here we report frequent activating mutations of STAT3 and STAT5B in NK/T-cell lymphomas (n - 51), gamma delta-T-cell lymphomas (n - 43) and their cell lines (n = 9) through next generation and/or Sanger sequencing. STAT5B N642H is particularly frequent in all forms of gamma delta-T-cell lymphomas. STAT3 and STAT5B mutations are associated with increased phosphorylated protein and a growth advantage to transduced cell lines or normal NK cells. Growth-promoting activity of the mutants can be partially inhibited by a JAK1/2 inhibitor. Molecular modelling and surface plasmon resonance measurements of the N642H mutant indicate a marked increase in binding affinity of the phosphotyrosine-Y699 with the mutant histidine. This is associated with the prolonged persistence of the mutant phosphoSTAT5B and marked increase of binding to target sites. Our findings suggest that JAK-STAT pathway inhibition may represent a therapeutic strategy.