Yazar "Ozer, Huseyin T. E." seçeneğine göre listele

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    Identification of Susceptibility Loci in IL6, RPS9/LILRB3, and an Intergenic Locus on Chromosome 21q22 in Takayasu Arteritis in a Genome-Wide Association Study
    (Wiley, 2015) Renauer, Paul A.; Saruhan-Direskeneli, Guher; Coit, Patrick; Adler, Adam; Aksu, Kenan; Keser, Gokhan; Alibaz-Oner, Fatma; Aydin, Sibel Z.; Kamali, Sevil; Inanc, Murat; Carette, Simon; Cuthbertson, David; Hoffman, Gary S.; Akar, Servet; Onen, Fatos; Akkoc, Nurullah; Khalidi, Nader A.; Koening, Curry; Karadag, Omer; Kiraz, Sedat; Langford, Carol A.; Maksimowicz-McKinnon, Kathleen; McAlear, Carol A.; Ozbalkan, Zeynep; Ates, Askin; Karaaslan, Yasar; Duzgun, Nursen; Monach, Paul A.; Ozer, Huseyin T. E.; Erken, Eren; Ozturk, Mehmet A.; Yazici, Ayten; Cefle, Ayse; Onat, Ahmet Mesut; Kisacik, Bunyamin; Pagnoux, Christian; Kasifoglu, Timucin; Seyahi, Emire; Fresko, Izzet; Seo, Philip; Sreih, Antoine G.; Warrington, Kenneth J.; Ytterberg, Steven R.; Cobankara, Veli; Cunninghame-Graham, Deborah S.; Vyse, Timothy J.; Pamuk, Omer N.; Tunc, S. Ercan; Dalkilic, Ediz; Bicakcigil, Muge; Yentur, Sibel P.; Wren, Jonathan D.; Merkel, Peter A.; Direskeneli, Haner; Sawalha, Amr H.
    Objective. Takayasu arteritis is a rare large vessel vasculitis with incompletely understood etiology. This study was undertaken to perform the first unbiased genome-wide association analysis of Takayasu arteritis. Methods. Two independent cohorts of patients with Takayasu arteritis from Turkey and North America were included in our study. The Turkish cohort consisted of 559 patients and 489 controls, and the North American cohort consisted of 134 patients and 1,047 controls of European ancestry. Genotyping was performed using the Omni1-Quad and Omni2.5 genotyping arrays. Genotyping data were subjected to rigorous quality control measures and subsequently analyzed to discover genetic susceptibility loci for Takayasu arteritis. Results. We identified genetic susceptibility loci for Takayasu arteritis with a genome-wide level of significance in IL6 (rs2069837) (odds ratio [OR] 2.07, P = 6.70 x 10(-9)), RPS9/LILRB3 (rs11666543) (OR 1.65, P = 2.34 x 10(-8)), and an intergenic locus on chromosome 21q22 (rs2836878) (OR 1.79, P = 3.62 x 10(-10)). The genetic susceptibility locus in RPS9/LILRB3 lies within the leukocyte receptor complex gene cluster on chromosome 19q13.4, and the disease risk variant in this locus correlates with reduced expression of multiple genes including the inhibitory leukocyte immunoglobulin-like receptor gene LILRB3 (P = 2.29 x 10(-8)). In addition, we identified candidate susceptibility genes with suggestive levels of association (P < 1 x 10(-5)) with Takayasu arteritis, including PCSK5, LILRA3, PPM1G/NRBP1, and PTK2B. Conclusion. Our findings indicate novel genetic susceptibility loci for Takayasu arteritis and uncover potentially important aspects of the pathophysiology of this form of vasculitis.
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    Identification of Susceptibility Loci in IL6, RPS9/LILRB3, and an Intergenic Locus on Chromosome 21q22 in Takayasu Arteritis in a Genome-Wide Association Study
    (Wiley, 2015) Renauer, Paul A.; Saruhan-Direskeneli, Guher; Coit, Patrick; Adler, Adam; Aksu, Kenan; Keser, Gokhan; Alibaz-Oner, Fatma; Aydin, Sibel Z.; Kamali, Sevil; Inanc, Murat; Carette, Simon; Cuthbertson, David; Hoffman, Gary S.; Akar, Servet; Onen, Fatos; Akkoc, Nurullah; Khalidi, Nader A.; Koening, Curry; Karadag, Omer; Kiraz, Sedat; Langford, Carol A.; Maksimowicz-McKinnon, Kathleen; McAlear, Carol A.; Ozbalkan, Zeynep; Ates, Askin; Karaaslan, Yasar; Duzgun, Nursen; Monach, Paul A.; Ozer, Huseyin T. E.; Erken, Eren; Ozturk, Mehmet A.; Yazici, Ayten; Cefle, Ayse; Onat, Ahmet Mesut; Kisacik, Bunyamin; Pagnoux, Christian; Kasifoglu, Timucin; Seyahi, Emire; Fresko, Izzet; Seo, Philip; Sreih, Antoine G.; Warrington, Kenneth J.; Ytterberg, Steven R.; Cobankara, Veli; Cunninghame-Graham, Deborah S.; Vyse, Timothy J.; Pamuk, Omer N.; Tunc, S. Ercan; Dalkilic, Ediz; Bicakcigil, Muge; Yentur, Sibel P.; Wren, Jonathan D.; Merkel, Peter A.; Direskeneli, Haner; Sawalha, Amr H.
    Objective. Takayasu arteritis is a rare large vessel vasculitis with incompletely understood etiology. This study was undertaken to perform the first unbiased genome-wide association analysis of Takayasu arteritis. Methods. Two independent cohorts of patients with Takayasu arteritis from Turkey and North America were included in our study. The Turkish cohort consisted of 559 patients and 489 controls, and the North American cohort consisted of 134 patients and 1,047 controls of European ancestry. Genotyping was performed using the Omni1-Quad and Omni2.5 genotyping arrays. Genotyping data were subjected to rigorous quality control measures and subsequently analyzed to discover genetic susceptibility loci for Takayasu arteritis. Results. We identified genetic susceptibility loci for Takayasu arteritis with a genome-wide level of significance in IL6 (rs2069837) (odds ratio [OR] 2.07, P = 6.70 x 10(-9)), RPS9/LILRB3 (rs11666543) (OR 1.65, P = 2.34 x 10(-8)), and an intergenic locus on chromosome 21q22 (rs2836878) (OR 1.79, P = 3.62 x 10(-10)). The genetic susceptibility locus in RPS9/LILRB3 lies within the leukocyte receptor complex gene cluster on chromosome 19q13.4, and the disease risk variant in this locus correlates with reduced expression of multiple genes including the inhibitory leukocyte immunoglobulin-like receptor gene LILRB3 (P = 2.29 x 10(-8)). In addition, we identified candidate susceptibility genes with suggestive levels of association (P < 1 x 10(-5)) with Takayasu arteritis, including PCSK5, LILRA3, PPM1G/NRBP1, and PTK2B. Conclusion. Our findings indicate novel genetic susceptibility loci for Takayasu arteritis and uncover potentially important aspects of the pathophysiology of this form of vasculitis.
  • Küçük Resim Yok
    Öğe
    Identification of Susceptibility Loci in IL6, RPS9/LILRB3, and an Intergenic Locus on Chromosome 21q22 in Takayasu Arteritis in a Genome-Wide Association Study
    (Wiley, 2015) Renauer, Paul A.; Saruhan-Direskeneli, Guher; Coit, Patrick; Adler, Adam; Aksu, Kenan; Keser, Gokhan; Alibaz-Oner, Fatma; Aydin, Sibel Z.; Kamali, Sevil; Inanc, Murat; Carette, Simon; Cuthbertson, David; Hoffman, Gary S.; Akar, Servet; Onen, Fatos; Akkoc, Nurullah; Khalidi, Nader A.; Koening, Curry; Karadag, Omer; Kiraz, Sedat; Langford, Carol A.; Maksimowicz-McKinnon, Kathleen; McAlear, Carol A.; Ozbalkan, Zeynep; Ates, Askin; Karaaslan, Yasar; Duzgun, Nursen; Monach, Paul A.; Ozer, Huseyin T. E.; Erken, Eren; Ozturk, Mehmet A.; Yazici, Ayten; Cefle, Ayse; Onat, Ahmet Mesut; Kisacik, Bunyamin; Pagnoux, Christian; Kasifoglu, Timucin; Seyahi, Emire; Fresko, Izzet; Seo, Philip; Sreih, Antoine G.; Warrington, Kenneth J.; Ytterberg, Steven R.; Cobankara, Veli; Cunninghame-Graham, Deborah S.; Vyse, Timothy J.; Pamuk, Omer N.; Tunc, S. Ercan; Dalkilic, Ediz; Bicakcigil, Muge; Yentur, Sibel P.; Wren, Jonathan D.; Merkel, Peter A.; Direskeneli, Haner; Sawalha, Amr H.
    Objective. Takayasu arteritis is a rare large vessel vasculitis with incompletely understood etiology. This study was undertaken to perform the first unbiased genome-wide association analysis of Takayasu arteritis. Methods. Two independent cohorts of patients with Takayasu arteritis from Turkey and North America were included in our study. The Turkish cohort consisted of 559 patients and 489 controls, and the North American cohort consisted of 134 patients and 1,047 controls of European ancestry. Genotyping was performed using the Omni1-Quad and Omni2.5 genotyping arrays. Genotyping data were subjected to rigorous quality control measures and subsequently analyzed to discover genetic susceptibility loci for Takayasu arteritis. Results. We identified genetic susceptibility loci for Takayasu arteritis with a genome-wide level of significance in IL6 (rs2069837) (odds ratio [OR] 2.07, P = 6.70 x 10(-9)), RPS9/LILRB3 (rs11666543) (OR 1.65, P = 2.34 x 10(-8)), and an intergenic locus on chromosome 21q22 (rs2836878) (OR 1.79, P = 3.62 x 10(-10)). The genetic susceptibility locus in RPS9/LILRB3 lies within the leukocyte receptor complex gene cluster on chromosome 19q13.4, and the disease risk variant in this locus correlates with reduced expression of multiple genes including the inhibitory leukocyte immunoglobulin-like receptor gene LILRB3 (P = 2.29 x 10(-8)). In addition, we identified candidate susceptibility genes with suggestive levels of association (P < 1 x 10(-5)) with Takayasu arteritis, including PCSK5, LILRA3, PPM1G/NRBP1, and PTK2B. Conclusion. Our findings indicate novel genetic susceptibility loci for Takayasu arteritis and uncover potentially important aspects of the pathophysiology of this form of vasculitis.
  • Küçük Resim Yok
    Öğe
    Takayasu's arteritis is associated with HLA-B*52, but not with HLA-B*51, in Turkey
    (Biomed Central Ltd, 2012) Sahin, Ziver; Bicakcigil, Muge; Aksu, Kenan; Kamali, Sevil; Akar, Servet; Onen, Fatos; Karadag, Omer; Ozbalkan, Zeynep; Ates, Askin; Ozer, Huseyin T. E.; Yilmaz, Vuslat; Seyahi, Emire; Ozturk, Mehmet A.; Cefle, Ayse; Cobankara, Veli; Onat, A. Mesut; Tunc, Ercan; Duzgun, Nursen; Aydin, Sibel Z.; Yilmaz, Neslihan; Fresko, Izzet; Karaaslan, Yasar; Kiraz, Sedat; Akkoc, Nurullah; Inanc, Murat; Keser, Gokhan; Uyar, F. Aytul; Direskeneli, Haner; Saruhan-Direskeneli, Guher
    Introduction: HLA-B*51 and HLA-B*52 are two close human leukocyte antigen (HLA) allele groups with minor amino acid differences. However, they are associated with two different vasculitides (HLA-B*51 in Beh et's disease and HLA-B*52 in Takayasu's arteritis (TAK)) and with major clinical and immunological differences. In this study, we aimed to screen a large cohort of TAK patients from Turkey for the presence of HLA-B*51 and HLA-B* 52 as susceptibility and severity factors. Methods: TAK patients (n = 330) followed at a total of 15 centers were included in the study. The mean age of the patients was 37.8 years, and 86% were women. DNA samples from the patients and healthy controls (HC; n = 210) were isolated, and the presence of HLA-B* 51 or HLA-B* 52 was screened for by using PCR with sequence-specific primers. Results: We found a significant association of HLA-B* 52 with TAK (20.9% vs HC = 6.7%, P = 0.000, OR = 3.7, 95% CI = 2.02 to 6.77). The distribution of HLA-B* 51 did not differ between TAK patients and HCs (22.7% vs 24.8%, OR = 0.9, 95% CI = 0.60 to 1.34). The presence of HLA-B* 52 decreased in late-onset patients (> 40 years of age; 12.0%, P = 0.024, OR = 0.43, 95% CI = 0.20 to 0.91). Patients with angiographic type I disease with limited aortic involvement also had a lower presence of HLA-B* 52 compared to those with all other disease subtypes (13.1% vs 26%, P = 0.005, OR = 0.43, 95% CI = 0.23 to 0.78). Conclusions: In this study, the previously reported association of TAK with HLA-B* 52 in other populations was confirmed in patients from Turkey. The functional relevance of HLA-B* 52 in TAK pathogenesis needs to be explored further.