<?xml version="1.0" encoding="UTF-8"?><OAI-PMH xmlns="http://www.openarchives.org/OAI/2.0/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/ http://www.openarchives.org/OAI/2.0/OAI-PMH.xsd"><responseDate>2026-10-19T01:56:15Z</responseDate><request verb="GetRecord" identifier="oai:ebyu-rdlopen.rawdatalibrary.net:ebyu/14623" metadataPrefix="oai_dc">https://ebyu-rdlopen.rawdatalibrary.net/oai/request</request><GetRecord><record><header><identifier>oai:ebyu-rdlopen.rawdatalibrary.net:ebyu/14623</identifier><datestamp>2026-10-18T21:14:24Z</datestamp><setSpec>openaire</setSpec><setSpec>driver</setSpec><setSpec>com_ebyu_10000</setSpec><setSpec>col_ebyu_10001</setSpec></header><metadata><oai_dc:dc xmlns:oai_dc="http://www.openarchives.org/OAI/2.0/oai_dc/" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/oai_dc/ http://www.openarchives.org/OAI/2.0/oai_dc.xsd"><dc:title>The Association of Plasminogen Activator Inhibitor Type 1 (PAI-1) Level and PAI-1 4G/5G Gene Polymorphism with the Formation and the Grade of Endometrial Cancer</dc:title><dc:creator>Yıldırım, Malik Ejder</dc:creator><dc:creator>Karakuş, Savas</dc:creator><dc:creator>Kurtulgan, Hande Küçük</dc:creator><dc:creator>Kılıçgün, Hasan</dc:creator><dc:creator>Erşan, Serpil</dc:creator><dc:creator>Bakır, Sevtap</dc:creator><dc:subject>Endometrial cancer</dc:subject><dc:subject>Grades</dc:subject><dc:subject>PAI-1 4G/5G polymorphism</dc:subject><dc:subject>PAI-1 levels</dc:subject><dc:subject>Adult</dc:subject><dc:subject>Aged</dc:subject><dc:subject>Endometrial Neoplasms</dc:subject><dc:subject>Female</dc:subject><dc:subject>Gene Expression Regulation, Neoplastic</dc:subject><dc:subject>Genetic Association Studies</dc:subject><dc:subject>Genetic Predisposition to Disease</dc:subject><dc:subject>Genotype</dc:subject><dc:subject>Humans</dc:subject><dc:subject>Middle Aged</dc:subject><dc:subject>Neoplasm Grading</dc:subject><dc:subject>Plasminogen Activator Inhibitor 1</dc:subject><dc:subject>Polymorphism, Single Nucleotide</dc:subject><dc:subject>Promoter Regions, Genetic</dc:subject><dc:subject>genomic DNA</dc:subject><dc:subject>SERPINE1 protein, human</dc:subject><dc:subject>allele</dc:subject><dc:subject>Article</dc:subject><dc:subject>body mass</dc:subject><dc:subject>cancer grading</dc:subject><dc:subject>cancer growth</dc:subject><dc:subject>cancer patient</dc:subject><dc:subject>carcinogenesis</dc:subject><dc:subject>controlled study</dc:subject><dc:subject>DNA polymorphism</dc:subject><dc:subject>endometrium carcinoma</dc:subject><dc:description>Plasminogen activator inhibitor type 1 (PAI-1) is a serine protease inhibitor (Serpine 1), and it inhibits both tissue plasminogen activator and urokinase plasminogen activator which are important in fibrinolysis. We aimed to find whether there is a possible association between PAI-1 level, PAI-1 4G/5G polymorphism, and endometrial cancer. PAI-1 levels in peripheral blood were determined in 82 patients with endometrial carcinoma and 76 female healthy controls using an enzyme-linked immunoassay (ELISA). Then, the genomic DNA was extracted and screened by reverse hybridization procedure (Strip assay) to detect PAI 1 4G/5G polymorphism. The levels of PAI-1 in the patients were higher statistically in comparison to controls (P &lt; 0.001). The distribution of PAI-1 4G/5G polymorphism was quite different between patients and controls (P = 0.008), and 4G allelic frequency was significantly higher in the patients of endometrial cancer than in controls (P = 0.026). We found significant difference between Grade 1 and Grade 2+3 patients in terms of the PAI-1 levels (P = 0.047). There was no association between PAI-1 4G/5G polymorphism and the grades of endometrial cancer (P = 0.993). Our data suggest that the level of PAI-1 and PAI-1 4G/5G gene polymorphism are effective in the formation of endometrial cancer. PAI-1 levels are also associated with the grades of endometrial cancer. © 2017, Springer Science+Business Media New York.</dc:description><dc:publisher>Springer New York LLC</dc:publisher><dc:date>2017</dc:date><dc:type>Article</dc:type><dc:identifier>https://rdlopen.rawdatalibrary.net/r/ebyu/14623</dc:identifier><dc:identifier>https://doi.org/10.1007/s10528-017-9796-7</dc:identifier><dc:identifier>0006-2928</dc:identifier><dc:language>en</dc:language><dc:relation>Biochemical Genetics</dc:relation><dc:rights>info:eu-repo/semantics/openAccess</dc:rights><dc:type>info:eu-repo/semantics/article</dc:type><dc:identifier>https://ebyu-rdlopen.rawdatalibrary.net/tr/items/ebyu/14623</dc:identifier></oai_dc:dc></metadata></record></GetRecord></OAI-PMH>