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<Article>
<Journal>
				<PublisherName>Isfahan University of Medical Sciences</PublisherName>
				<JournalTitle>Journal of Isfahan Medical School</JournalTitle>
				<Issn>1027-7595</Issn>
				<Volume>30</Volume>
				<Issue>205</Issue>
				<PubDate PubStatus="epublish">
					<Year>2012</Year>
					<Month>10</Month>
					<Day>22</Day>
				</PubDate>
			</Journal>
<ArticleTitle>The Association between Gelatinase B and Lung Cancer in Smokers and Non-Smokers</ArticleTitle>
<VernacularTitle>The Association between Gelatinase B and Lung Cancer in Smokers and Non-Smokers</VernacularTitle>
			<FirstPage></FirstPage>
			<LastPage></LastPage>
			<ELocationID EIdType="pii">13882</ELocationID>
			
			
			<Language>FA</Language>
<AuthorList>
<Author>
					<FirstName>Majid</FirstName>
					<LastName>Motovali-Bashi</LastName>
<Affiliation>Assistant Professor, Department of Biology, School of Sciences, University of Isfahan, Isfahan, Iran</Affiliation>
<Identifier Source="ORCID">0000-0003-4380-0166</Identifier>

</Author>
<Author>
					<FirstName>Simin</FirstName>
					<LastName>Hemmati</LastName>
<Affiliation>Assistant Professor, Department of Oncology and Radiotherapy, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran</Affiliation>
<Identifier Source="ORCID">0000-0001-7517-8987</Identifier>

</Author>
<Author>
					<FirstName>Somayeh</FirstName>
					<LastName>Taghvaei</LastName>
<Affiliation>MSc Student, Department of Biology, School of Sciences, University of Isfahan, Isfahan, Iran</Affiliation>

</Author>
</AuthorList>
				<PublicationType>Journal Article</PublicationType>
			<History>
				<PubDate PubStatus="received">
					<Year>2011</Year>
					<Month>11</Month>
					<Day>29</Day>
				</PubDate>
			</History>
		<Abstract>Background: Gelatinase B is not only involved in metastasis, but also alters and processes growth factors, growth factor receptors, angiogenic factors, and other proteinases and thus affects early carcinogenesis. In other words, it has a fundamental role in initiation and development of cancer. Genetic polymorphism in the promoter of gelatinase B has been reported to be associated with the risk of several cancers including lung cancer. Methods: Genotyping of gelatinase B was carried out by taking blood samples from 172 patients with lung cancer and 100 controls using restriction fragment length polymorphism-polymerase chain reaction (RFLP-PCR) technique. The observed numbers of each gelatinase B genotype were compared with that expected for a population in Hardy-Weinberg equilibrium by χ2 test. The significance of the differences of the observed alleles and genotypes between groups was tested using the odds ratio (OR) analysis. Findings: The percentage of smokers in patients was more than controls (57.5% vs. 30%). Distribution of gelatinase B genotype was significantly associated with the risk of lung cancer [OR = 2.56; 95% confidence interval (CI) = 0.06-23.82]. Conclusion: Our results indicated that smokers who carry TT and CT+TT genotypes have 4 (OR = 3.45; 95% CI = 1.28-9.24) and 15 (OR = 14.66; 95% CI = 3.95-53.47) fold risks of lung cancer, respectively. Keywords: Gelatinase B, Restriction fragment length polymorphism, Polymerase chain reaction, Genotyping, Smokers, Lung cancer</Abstract>
			<OtherAbstract Language="FA">Background: Gelatinase B is not only involved in metastasis, but also alters and processes growth factors, growth factor receptors, angiogenic factors, and other proteinases and thus affects early carcinogenesis. In other words, it has a fundamental role in initiation and development of cancer. Genetic polymorphism in the promoter of gelatinase B has been reported to be associated with the risk of several cancers including lung cancer. Methods: Genotyping of gelatinase B was carried out by taking blood samples from 172 patients with lung cancer and 100 controls using restriction fragment length polymorphism-polymerase chain reaction (RFLP-PCR) technique. The observed numbers of each gelatinase B genotype were compared with that expected for a population in Hardy-Weinberg equilibrium by χ2 test. The significance of the differences of the observed alleles and genotypes between groups was tested using the odds ratio (OR) analysis. Findings: The percentage of smokers in patients was more than controls (57.5% vs. 30%). Distribution of gelatinase B genotype was significantly associated with the risk of lung cancer [OR = 2.56; 95% confidence interval (CI) = 0.06-23.82]. Conclusion: Our results indicated that smokers who carry TT and CT+TT genotypes have 4 (OR = 3.45; 95% CI = 1.28-9.24) and 15 (OR = 14.66; 95% CI = 3.95-53.47) fold risks of lung cancer, respectively. Keywords: Gelatinase B, Restriction fragment length polymorphism, Polymerase chain reaction, Genotyping, Smokers, Lung cancer</OtherAbstract>
<ArchiveCopySource DocType="pdf">https://jims.mui.ac.ir/article_13882_b7cda51a7b31b77fe2d5c1ee19f33496.pdf</ArchiveCopySource>
</Article>
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