<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>12(8)</volume><submitter>Cui M</submitter><pubmed_abstract>BACKGROUND &amp; AIMS:Primary hepatic cancer (PHC) is a common malignant tumor and the third most frequent cause of cancer-related death worldwide. However, the molecular mechanisms underlying hepatic cancer remain unknown. CTSB is considered a biomarker of cancer as it can facilitate tumor progression. We aimed to investigate the association between genetic polymorphisms of potential regulatory SNPs in the CTSB gene and PHC. METHODS:The relationship between CTSB rs12898 and PHC was analyzed in a case-control study with a Chinese population of 608 PHC patients and 608 healthy individuals using SPSS 21.0. RESULTS:PHC was significantly associated with alcohol consumption (P &lt; 0.001), history of hepatitis (P &lt; 0.001), and liver cirrhosis (P &lt; 0.001), but not with smoking (P = 0.168), age (P = 0.175), or sex (P = 0.051). Distribution of three genotypes (GG, GA, and AA) of CTSB rs12898 significantly differed between the cases and controls (P &lt; 0.001). Compared with the GG genotype, the GA and AA genotype was associated with a significantly increased risk of PHC (OR = 1.425, 95% CI = 1.099-1.848, P = 0.007; and OR = 2.220, 95% CI = 1.574-3.132, P &lt; 0.001, respectively). CTSB rs12898 was associated with a significantly increased risk of PHC under a dominant model (OR = 1.592, 95% CI = 1.243-2.040, P &lt; 0.001), and under a recessive model (OR = 1.771, 95% CI = 1.311-2.393, P &lt; 0.001) for the variant A allele. CONCLUSION:Results suggest that CTSB rs12898G > A may play a role in the pathogenesis of PHC, and may be a marker for susceptibility to PHC.</pubmed_abstract><journal>International journal of clinical and experimental pathology</journal><pagination>3063-3069</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC6949695</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>A single nucleotide polymorphism CTSB rs12898 is associated with primary hepatic cancer in a Chinese population.</pubmed_title><pmcid>PMC6949695</pmcid><pubmed_authors>Cui M</pubmed_authors><pubmed_authors>Chen Q</pubmed_authors><pubmed_authors>He C</pubmed_authors><pubmed_authors>Jin S</pubmed_authors><pubmed_authors>Lin Z</pubmed_authors><pubmed_authors>Sun Z</pubmed_authors><pubmed_authors>Cui Q</pubmed_authors><pubmed_authors>Wang N</pubmed_authors><pubmed_authors>Jin G</pubmed_authors><pubmed_authors>Lee SY</pubmed_authors><pubmed_authors>Park JY</pubmed_authors><pubmed_authors>Cui H</pubmed_authors><pubmed_authors>Yu Y</pubmed_authors></additional><is_claimable>false</is_claimable><name>A single nucleotide polymorphism CTSB rs12898 is associated with primary hepatic cancer in a Chinese population.</name><description>BACKGROUND &amp; AIMS:Primary hepatic cancer (PHC) is a common malignant tumor and the third most frequent cause of cancer-related death worldwide. However, the molecular mechanisms underlying hepatic cancer remain unknown. CTSB is considered a biomarker of cancer as it can facilitate tumor progression. We aimed to investigate the association between genetic polymorphisms of potential regulatory SNPs in the CTSB gene and PHC. METHODS:The relationship between CTSB rs12898 and PHC was analyzed in a case-control study with a Chinese population of 608 PHC patients and 608 healthy individuals using SPSS 21.0. RESULTS:PHC was significantly associated with alcohol consumption (P &lt; 0.001), history of hepatitis (P &lt; 0.001), and liver cirrhosis (P &lt; 0.001), but not with smoking (P = 0.168), age (P = 0.175), or sex (P = 0.051). Distribution of three genotypes (GG, GA, and AA) of CTSB rs12898 significantly differed between the cases and controls (P &lt; 0.001). Compared with the GG genotype, the GA and AA genotype was associated with a significantly increased risk of PHC (OR = 1.425, 95% CI = 1.099-1.848, P = 0.007; and OR = 2.220, 95% CI = 1.574-3.132, P &lt; 0.001, respectively). CTSB rs12898 was associated with a significantly increased risk of PHC under a dominant model (OR = 1.592, 95% CI = 1.243-2.040, P &lt; 0.001), and under a recessive model (OR = 1.771, 95% CI = 1.311-2.393, P &lt; 0.001) for the variant A allele. CONCLUSION:Results suggest that CTSB rs12898G > A may play a role in the pathogenesis of PHC, and may be a marker for susceptibility to PHC.</description><dates><release>2019-01-01T00:00:00Z</release><publication>2019</publication><modification>2024-02-15T21:53:27.638Z</modification><creation>2020-11-08T09:58:03Z</creation></dates><accession>S-EPMC6949695</accession><cross_references><pubmed>31934146</pubmed></cross_references></HashMap>