Association of polymorphisms in MALAT1 with the risk of endometrial cancer in Southern Chinese women

Background Endometrial cancer is the most common gynecologic malignancy worldwide. Polymorphisms in MALAT1 have been demonstrated to play critical roles in cancer. However, the roles of MALAT1 polymorphisms in the etiology of endometrial cancer have not been well documented. Methods We genotyped thr...

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Veröffentlicht in:Journal of clinical laboratory analysis 2020-04, Vol.34 (4), p.e23146-n/a
Hauptverfasser: Chen, Guange, Zhang, Mingyao, Liang, Zongwen, Chen, Sailing, Chen, Feng, Zhu, Jiawei, Zhao, Manman, He, Jing, Hua, Wenfeng, Duan, Ping
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container_issue 4
container_start_page e23146
container_title Journal of clinical laboratory analysis
container_volume 34
creator Chen, Guange
Zhang, Mingyao
Liang, Zongwen
Chen, Sailing
Chen, Feng
Zhu, Jiawei
Zhao, Manman
He, Jing
Hua, Wenfeng
Duan, Ping
description Background Endometrial cancer is the most common gynecologic malignancy worldwide. Polymorphisms in MALAT1 have been demonstrated to play critical roles in cancer. However, the roles of MALAT1 polymorphisms in the etiology of endometrial cancer have not been well documented. Methods We genotyped three MALAT1 polymorphisms in 249 endometrial cancer cases and 446 cancer‐free female controls using quantitative polymerase chain reaction with TaqMan probes. To estimate the association between MALAT1 polymorphisms (rs591291 C>T, rs664589 C>G, and rs4102217 G>C) and the risk of endometrial cancer, an unconditional logistic regression model was conducted to calculate the odds ratio (OR) and the 95% confidence interval (CI), adjusting for surgery history, menopause, number of deliveries, BMI, and FIGO stage. Results We found that the MALAT1 rs664589 C>G polymorphism was significantly associated with endometrial cancer risk (heterogeneous: adjusted OR = 0.57, 95% CI = 0.34‐0.93, P = .026; homogenous: adjusted OR = 3.74, 95% CI = 1.12‐12.45, P = .032; and recessive: adjusted OR = 4.06, 95% CI = 1.22‐13.48, P = .022). Stratified analysis further demonstrated that the MALAT1 rs664589 C>G polymorphism significantly increased the risk of endometrial cancer susceptibility in patients with no history of surgery, more deliveries, BMI between 25 and 29.9, and FIGO stages II‐III. Compared with the wild‐type GCG haplotype carriers, individuals with CGG haplotypes had a higher risk of developing endometrial cancer. Conclusion The MALAT1 rs664589 C>G polymorphism was associated with a significant increase in endometrial cancer risk.
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Polymorphisms in MALAT1 have been demonstrated to play critical roles in cancer. However, the roles of MALAT1 polymorphisms in the etiology of endometrial cancer have not been well documented. Methods We genotyped three MALAT1 polymorphisms in 249 endometrial cancer cases and 446 cancer‐free female controls using quantitative polymerase chain reaction with TaqMan probes. To estimate the association between MALAT1 polymorphisms (rs591291 C&gt;T, rs664589 C&gt;G, and rs4102217 G&gt;C) and the risk of endometrial cancer, an unconditional logistic regression model was conducted to calculate the odds ratio (OR) and the 95% confidence interval (CI), adjusting for surgery history, menopause, number of deliveries, BMI, and FIGO stage. Results We found that the MALAT1 rs664589 C&gt;G polymorphism was significantly associated with endometrial cancer risk (heterogeneous: adjusted OR = 0.57, 95% CI = 0.34‐0.93, P = .026; homogenous: adjusted OR = 3.74, 95% CI = 1.12‐12.45, P = .032; and recessive: adjusted OR = 4.06, 95% CI = 1.22‐13.48, P = .022). Stratified analysis further demonstrated that the MALAT1 rs664589 C&gt;G polymorphism significantly increased the risk of endometrial cancer susceptibility in patients with no history of surgery, more deliveries, BMI between 25 and 29.9, and FIGO stages II‐III. Compared with the wild‐type GCG haplotype carriers, individuals with CGG haplotypes had a higher risk of developing endometrial cancer. Conclusion The MALAT1 rs664589 C&gt;G polymorphism was associated with a significant increase in endometrial cancer risk.</description><identifier>ISSN: 0887-8013</identifier><identifier>EISSN: 1098-2825</identifier><identifier>DOI: 10.1002/jcla.23146</identifier><identifier>PMID: 31880028</identifier><language>eng</language><publisher>United States: John Wiley &amp; Sons, Inc</publisher><subject>Adult ; Age ; Aged ; Aged, 80 and over ; Asian Continental Ancestry Group - genetics ; Cancer ; Case-Control Studies ; Confidence intervals ; Deoxyribonucleic acid ; DNA ; Endometrial cancer ; Endometrial Neoplasms - genetics ; Endometrium ; Etiology ; Female ; Genetic Association Studies ; Genetic Predisposition to Disease ; Genotype &amp; phenotype ; Haplotypes ; Haplotypes - genetics ; Health risk assessment ; Humans ; Logistic Models ; MALAT1 ; Malignancy ; Menopause ; Metastasis ; Middle Aged ; Polymerase chain reaction ; Polymorphism, Single Nucleotide - genetics ; risk ; Risk Factors ; RNA, Long Noncoding - genetics ; single nucleotide polymorphisms ; Surgery ; Womens health</subject><ispartof>Journal of clinical laboratory analysis, 2020-04, Vol.34 (4), p.e23146-n/a</ispartof><rights>2019 The Authors. published by Wiley Periodicals, Inc.</rights><rights>2019 The Authors. Journal of Clinical Laboratory Analysis published by Wiley Periodicals, Inc.</rights><rights>2020. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4486-136febaa673b5b2f3b867fe399831f1622c46e1a7cb06d18618e32d64ac6e0913</citedby><cites>FETCH-LOGICAL-c4486-136febaa673b5b2f3b867fe399831f1622c46e1a7cb06d18618e32d64ac6e0913</cites><orcidid>0000-0002-1954-2892 ; 0000-0003-0177-182X</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7171330/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7171330/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,1411,11541,27901,27902,45550,45551,46027,46451,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31880028$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chen, Guange</creatorcontrib><creatorcontrib>Zhang, Mingyao</creatorcontrib><creatorcontrib>Liang, Zongwen</creatorcontrib><creatorcontrib>Chen, Sailing</creatorcontrib><creatorcontrib>Chen, Feng</creatorcontrib><creatorcontrib>Zhu, Jiawei</creatorcontrib><creatorcontrib>Zhao, Manman</creatorcontrib><creatorcontrib>He, Jing</creatorcontrib><creatorcontrib>Hua, Wenfeng</creatorcontrib><creatorcontrib>Duan, Ping</creatorcontrib><title>Association of polymorphisms in MALAT1 with the risk of endometrial cancer in Southern Chinese women</title><title>Journal of clinical laboratory analysis</title><addtitle>J Clin Lab Anal</addtitle><description>Background Endometrial cancer is the most common gynecologic malignancy worldwide. Polymorphisms in MALAT1 have been demonstrated to play critical roles in cancer. However, the roles of MALAT1 polymorphisms in the etiology of endometrial cancer have not been well documented. Methods We genotyped three MALAT1 polymorphisms in 249 endometrial cancer cases and 446 cancer‐free female controls using quantitative polymerase chain reaction with TaqMan probes. To estimate the association between MALAT1 polymorphisms (rs591291 C&gt;T, rs664589 C&gt;G, and rs4102217 G&gt;C) and the risk of endometrial cancer, an unconditional logistic regression model was conducted to calculate the odds ratio (OR) and the 95% confidence interval (CI), adjusting for surgery history, menopause, number of deliveries, BMI, and FIGO stage. Results We found that the MALAT1 rs664589 C&gt;G polymorphism was significantly associated with endometrial cancer risk (heterogeneous: adjusted OR = 0.57, 95% CI = 0.34‐0.93, P = .026; homogenous: adjusted OR = 3.74, 95% CI = 1.12‐12.45, P = .032; and recessive: adjusted OR = 4.06, 95% CI = 1.22‐13.48, P = .022). Stratified analysis further demonstrated that the MALAT1 rs664589 C&gt;G polymorphism significantly increased the risk of endometrial cancer susceptibility in patients with no history of surgery, more deliveries, BMI between 25 and 29.9, and FIGO stages II‐III. Compared with the wild‐type GCG haplotype carriers, individuals with CGG haplotypes had a higher risk of developing endometrial cancer. Conclusion The MALAT1 rs664589 C&gt;G polymorphism was associated with a significant increase in endometrial cancer risk.</description><subject>Adult</subject><subject>Age</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Asian Continental Ancestry Group - genetics</subject><subject>Cancer</subject><subject>Case-Control Studies</subject><subject>Confidence intervals</subject><subject>Deoxyribonucleic acid</subject><subject>DNA</subject><subject>Endometrial cancer</subject><subject>Endometrial Neoplasms - genetics</subject><subject>Endometrium</subject><subject>Etiology</subject><subject>Female</subject><subject>Genetic Association Studies</subject><subject>Genetic Predisposition to Disease</subject><subject>Genotype &amp; phenotype</subject><subject>Haplotypes</subject><subject>Haplotypes - genetics</subject><subject>Health risk assessment</subject><subject>Humans</subject><subject>Logistic Models</subject><subject>MALAT1</subject><subject>Malignancy</subject><subject>Menopause</subject><subject>Metastasis</subject><subject>Middle Aged</subject><subject>Polymerase chain reaction</subject><subject>Polymorphism, Single Nucleotide - genetics</subject><subject>risk</subject><subject>Risk Factors</subject><subject>RNA, Long Noncoding - genetics</subject><subject>single nucleotide polymorphisms</subject><subject>Surgery</subject><subject>Womens health</subject><issn>0887-8013</issn><issn>1098-2825</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp90U-L1DAYBvAgijuuXvwAEvCyCF3zJm2aXoQy-JcRD67nkKZvbcY2GZPWYb69rbMu6sFTDvnl4QkPIU-BXQNj_OXeDuaaC8jlPbIBVqmMK17cJxumVJkpBuKCPEppzxhTFciH5EKAUstLtSFtnVKwzkwueBo6egjDaQzx0Ls0Juo8_Vjv6hugRzf1dOqRRpe-rRB9G0acojMDtcZbjKv-HOYFRU-3vfOYkB4X5B-TB50ZEj65PS_Jlzevb7bvst2nt--39S6zea5kBkJ22BgjS9EUDe9Eo2TZoagqJaADybnNJYIpbcNkC0qCQsFbmRsrkVUgLsmrc-5hbkZsLfopmkEfohtNPOlgnP77xrtefw0_dAklCMGWgKvbgBi-z5gmPbpkcRiMxzAnzYUAXixN8oU-_4fuwxz98r1FVRyKqixW9eKsbAwpRezuygDT63h6HU__Gm_Bz_6sf0d_r7UAOIOjG_D0nyj9Yburz6E_AW06pNA</recordid><startdate>202004</startdate><enddate>202004</enddate><creator>Chen, Guange</creator><creator>Zhang, Mingyao</creator><creator>Liang, Zongwen</creator><creator>Chen, Sailing</creator><creator>Chen, Feng</creator><creator>Zhu, Jiawei</creator><creator>Zhao, Manman</creator><creator>He, Jing</creator><creator>Hua, Wenfeng</creator><creator>Duan, Ping</creator><general>John Wiley &amp; 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Zhang, Mingyao ; Liang, Zongwen ; Chen, Sailing ; Chen, Feng ; Zhu, Jiawei ; Zhao, Manman ; He, Jing ; Hua, Wenfeng ; Duan, Ping</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4486-136febaa673b5b2f3b867fe399831f1622c46e1a7cb06d18618e32d64ac6e0913</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Adult</topic><topic>Age</topic><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Asian Continental Ancestry Group - genetics</topic><topic>Cancer</topic><topic>Case-Control Studies</topic><topic>Confidence intervals</topic><topic>Deoxyribonucleic acid</topic><topic>DNA</topic><topic>Endometrial cancer</topic><topic>Endometrial Neoplasms - genetics</topic><topic>Endometrium</topic><topic>Etiology</topic><topic>Female</topic><topic>Genetic Association Studies</topic><topic>Genetic Predisposition to Disease</topic><topic>Genotype &amp; phenotype</topic><topic>Haplotypes</topic><topic>Haplotypes - genetics</topic><topic>Health risk assessment</topic><topic>Humans</topic><topic>Logistic Models</topic><topic>MALAT1</topic><topic>Malignancy</topic><topic>Menopause</topic><topic>Metastasis</topic><topic>Middle Aged</topic><topic>Polymerase chain reaction</topic><topic>Polymorphism, Single Nucleotide - genetics</topic><topic>risk</topic><topic>Risk Factors</topic><topic>RNA, Long Noncoding - genetics</topic><topic>single nucleotide polymorphisms</topic><topic>Surgery</topic><topic>Womens health</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chen, Guange</creatorcontrib><creatorcontrib>Zhang, Mingyao</creatorcontrib><creatorcontrib>Liang, Zongwen</creatorcontrib><creatorcontrib>Chen, Sailing</creatorcontrib><creatorcontrib>Chen, Feng</creatorcontrib><creatorcontrib>Zhu, Jiawei</creatorcontrib><creatorcontrib>Zhao, Manman</creatorcontrib><creatorcontrib>He, Jing</creatorcontrib><creatorcontrib>Hua, Wenfeng</creatorcontrib><creatorcontrib>Duan, Ping</creatorcontrib><collection>Wiley Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Calcium &amp; 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Medical Complete (Alumni)</collection><collection>Biological Sciences</collection><collection>Health &amp; Medical Collection (Alumni Edition)</collection><collection>Biological Science Database</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of clinical laboratory analysis</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chen, Guange</au><au>Zhang, Mingyao</au><au>Liang, Zongwen</au><au>Chen, Sailing</au><au>Chen, Feng</au><au>Zhu, Jiawei</au><au>Zhao, Manman</au><au>He, Jing</au><au>Hua, Wenfeng</au><au>Duan, Ping</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Association of polymorphisms in MALAT1 with the risk of endometrial cancer in Southern Chinese women</atitle><jtitle>Journal of clinical laboratory analysis</jtitle><addtitle>J Clin Lab Anal</addtitle><date>2020-04</date><risdate>2020</risdate><volume>34</volume><issue>4</issue><spage>e23146</spage><epage>n/a</epage><pages>e23146-n/a</pages><issn>0887-8013</issn><eissn>1098-2825</eissn><abstract>Background Endometrial cancer is the most common gynecologic malignancy worldwide. Polymorphisms in MALAT1 have been demonstrated to play critical roles in cancer. However, the roles of MALAT1 polymorphisms in the etiology of endometrial cancer have not been well documented. Methods We genotyped three MALAT1 polymorphisms in 249 endometrial cancer cases and 446 cancer‐free female controls using quantitative polymerase chain reaction with TaqMan probes. To estimate the association between MALAT1 polymorphisms (rs591291 C&gt;T, rs664589 C&gt;G, and rs4102217 G&gt;C) and the risk of endometrial cancer, an unconditional logistic regression model was conducted to calculate the odds ratio (OR) and the 95% confidence interval (CI), adjusting for surgery history, menopause, number of deliveries, BMI, and FIGO stage. Results We found that the MALAT1 rs664589 C&gt;G polymorphism was significantly associated with endometrial cancer risk (heterogeneous: adjusted OR = 0.57, 95% CI = 0.34‐0.93, P = .026; homogenous: adjusted OR = 3.74, 95% CI = 1.12‐12.45, P = .032; and recessive: adjusted OR = 4.06, 95% CI = 1.22‐13.48, P = .022). Stratified analysis further demonstrated that the MALAT1 rs664589 C&gt;G polymorphism significantly increased the risk of endometrial cancer susceptibility in patients with no history of surgery, more deliveries, BMI between 25 and 29.9, and FIGO stages II‐III. Compared with the wild‐type GCG haplotype carriers, individuals with CGG haplotypes had a higher risk of developing endometrial cancer. Conclusion The MALAT1 rs664589 C&gt;G polymorphism was associated with a significant increase in endometrial cancer risk.</abstract><cop>United States</cop><pub>John Wiley &amp; Sons, Inc</pub><pmid>31880028</pmid><doi>10.1002/jcla.23146</doi><tpages>7</tpages><orcidid>https://orcid.org/0000-0002-1954-2892</orcidid><orcidid>https://orcid.org/0000-0003-0177-182X</orcidid><oa>free_for_read</oa></addata></record>
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subjects Adult
Age
Aged
Aged, 80 and over
Asian Continental Ancestry Group - genetics
Cancer
Case-Control Studies
Confidence intervals
Deoxyribonucleic acid
DNA
Endometrial cancer
Endometrial Neoplasms - genetics
Endometrium
Etiology
Female
Genetic Association Studies
Genetic Predisposition to Disease
Genotype & phenotype
Haplotypes
Haplotypes - genetics
Health risk assessment
Humans
Logistic Models
MALAT1
Malignancy
Menopause
Metastasis
Middle Aged
Polymerase chain reaction
Polymorphism, Single Nucleotide - genetics
risk
Risk Factors
RNA, Long Noncoding - genetics
single nucleotide polymorphisms
Surgery
Womens health
title Association of polymorphisms in MALAT1 with the risk of endometrial cancer in Southern Chinese women
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