Contributions of NFKB1 ‐94insertion/deletion ATTG polymorphism to the susceptibility of gastrointestinal cancers: A meta‐analysis
Nuclear factor‐kappa B1 (NF‐κB1), a pleiotropic transcription factor, functions as a critical contributor to tumorigenesis. Growing numbers of case‐control studies were carried out to analyse the potential contribution of NF‐κB1 gene variants to gastrointestinal cancer risk, yet remains conflicting...
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| Veröffentlicht in: | Journal of cellular and molecular medicine 2021-11, Vol.25 (22), p.10674-10683 |
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| description | Nuclear factor‐kappa B1 (NF‐κB1), a pleiotropic transcription factor, functions as a critical contributor to tumorigenesis. Growing numbers of case‐control studies were carried out to analyse the potential contribution of NF‐κB1 gene variants to gastrointestinal cancer risk, yet remains conflicting conclusions. Therefore, we conducted this most up‐to‐date meta‐analysis to evaluate the relationship between NF‐κB1 gene insertion (I)/deletion (D) polymorphism, namely −94ins/delATTG or rs28362491, and the susceptibility to gastrointestinal cancers. We searched PubMed, EMBASE and MEDLINE databases updated in April 2021 for relevant studies. Meta‐analysis was carried out by software Stata11.0. The quantification of the relationship was determined by computing the combined odds ratios (ORs) and their corresponding 95% confidence intervals (CIs). Sensitivity analysis, the funnel plot and Begg's rank correlation test were also applied. Our findings indicate that −94ins/delATTG polymorphism could not significantly impact the susceptibility to gastrointestinal cancers. Under any five genetic models, −94ins/delATTG polymorphism was not remarkedly linked to the risk of colorectal, gastric and oesophageal cancer, respectively. The significant role of −94ins/delATTG was only observed in some certain subgroups. Findings here suggest that NF‐κB1 gene −94ins/delATTG polymorphism may not predispose to gastrointestinal cancer susceptibility. |
| doi_str_mv | 10.1111/jcmm.17004 |
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Growing numbers of case‐control studies were carried out to analyse the potential contribution of NF‐κB1 gene variants to gastrointestinal cancer risk, yet remains conflicting conclusions. Therefore, we conducted this most up‐to‐date meta‐analysis to evaluate the relationship between NF‐κB1 gene insertion (I)/deletion (D) polymorphism, namely −94ins/delATTG or rs28362491, and the susceptibility to gastrointestinal cancers. We searched PubMed, EMBASE and MEDLINE databases updated in April 2021 for relevant studies. Meta‐analysis was carried out by software Stata11.0. The quantification of the relationship was determined by computing the combined odds ratios (ORs) and their corresponding 95% confidence intervals (CIs). Sensitivity analysis, the funnel plot and Begg's rank correlation test were also applied. Our findings indicate that −94ins/delATTG polymorphism could not significantly impact the susceptibility to gastrointestinal cancers. Under any five genetic models, −94ins/delATTG polymorphism was not remarkedly linked to the risk of colorectal, gastric and oesophageal cancer, respectively. The significant role of −94ins/delATTG was only observed in some certain subgroups. Findings here suggest that NF‐κB1 gene −94ins/delATTG polymorphism may not predispose to gastrointestinal cancer susceptibility.</description><identifier>ISSN: 1582-1838</identifier><identifier>ISSN: 1582-4934</identifier><identifier>EISSN: 1582-4934</identifier><identifier>DOI: 10.1111/jcmm.17004</identifier><identifier>PMID: 34672421</identifier><language>eng</language><publisher>England: John Wiley & Sons, Inc</publisher><subject>Alleles ; Cancer ; Colorectal cancer ; Esophageal cancer ; Esophagus ; Ethnicity ; Gastric cancer ; Gastrointestinal cancer ; gastrointestinal cancers ; Gastrointestinal Neoplasms - diagnosis ; Gastrointestinal Neoplasms - epidemiology ; Gastrointestinal Neoplasms - etiology ; Gene deletion ; Gene polymorphism ; Genetic Association Studies ; Genetic Predisposition to Disease ; Humans ; Insertion ; Meta-analysis ; Mutagenesis, Insertional ; NF-kappa B p50 Subunit - genetics ; NF‐κB1 ; Odds Ratio ; Original ; Polymerase chain reaction ; Polymorphism ; Polymorphism, Genetic ; Publication Bias ; Sensitivity analysis ; Sequence Deletion ; SNPs ; Susceptibility ; Tumorigenesis</subject><ispartof>Journal of cellular and molecular medicine, 2021-11, Vol.25 (22), p.10674-10683</ispartof><rights>2021 The Authors. published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.</rights><rights>2021 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.</rights><rights>2021. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). 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Growing numbers of case‐control studies were carried out to analyse the potential contribution of NF‐κB1 gene variants to gastrointestinal cancer risk, yet remains conflicting conclusions. Therefore, we conducted this most up‐to‐date meta‐analysis to evaluate the relationship between NF‐κB1 gene insertion (I)/deletion (D) polymorphism, namely −94ins/delATTG or rs28362491, and the susceptibility to gastrointestinal cancers. We searched PubMed, EMBASE and MEDLINE databases updated in April 2021 for relevant studies. Meta‐analysis was carried out by software Stata11.0. The quantification of the relationship was determined by computing the combined odds ratios (ORs) and their corresponding 95% confidence intervals (CIs). Sensitivity analysis, the funnel plot and Begg's rank correlation test were also applied. Our findings indicate that −94ins/delATTG polymorphism could not significantly impact the susceptibility to gastrointestinal cancers. Under any five genetic models, −94ins/delATTG polymorphism was not remarkedly linked to the risk of colorectal, gastric and oesophageal cancer, respectively. The significant role of −94ins/delATTG was only observed in some certain subgroups. Findings here suggest that NF‐κB1 gene −94ins/delATTG polymorphism may not predispose to gastrointestinal cancer susceptibility.</description><subject>Alleles</subject><subject>Cancer</subject><subject>Colorectal cancer</subject><subject>Esophageal cancer</subject><subject>Esophagus</subject><subject>Ethnicity</subject><subject>Gastric cancer</subject><subject>Gastrointestinal cancer</subject><subject>gastrointestinal cancers</subject><subject>Gastrointestinal Neoplasms - diagnosis</subject><subject>Gastrointestinal Neoplasms - epidemiology</subject><subject>Gastrointestinal Neoplasms - etiology</subject><subject>Gene deletion</subject><subject>Gene polymorphism</subject><subject>Genetic Association Studies</subject><subject>Genetic Predisposition to Disease</subject><subject>Humans</subject><subject>Insertion</subject><subject>Meta-analysis</subject><subject>Mutagenesis, Insertional</subject><subject>NF-kappa B p50 Subunit - genetics</subject><subject>NF‐κB1</subject><subject>Odds Ratio</subject><subject>Original</subject><subject>Polymerase chain reaction</subject><subject>Polymorphism</subject><subject>Polymorphism, Genetic</subject><subject>Publication Bias</subject><subject>Sensitivity analysis</subject><subject>Sequence Deletion</subject><subject>SNPs</subject><subject>Susceptibility</subject><subject>Tumorigenesis</subject><issn>1582-1838</issn><issn>1582-4934</issn><issn>1582-4934</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp9kc1u1DAUhS0EoqWw4QGQJTYIaVr_3EwcFkjTEW2BFjbD2vI4TscjJ05tpyg7Nux5Rp6kDjNUwAJvfOX76fgcHYSeU3JM8znZ6rY9piUh8AAd0kKwGVQcHu5nKrg4QE9i3BLC55RXj9EBh3nJgNFD9H3puxTsekjWdxH7Bn86-3hK8c9vPyqwXTRhWpzUxplpwIvV6hz33o2tD_3GxhYnj9PG4DhEbfpk19bZNE5C1yqm4G2XTEy2Uw5r1WkT4hu8wK1JKn-h8vMYbXyKHjXKRfNsfx-hL2fvVsuL2eXn8_fLxeVMAwiYKUpYs9Y1rYArDnyuTMNLznhZs5y1AFZzQ4iogNBGlMTUoA3ootB1qYEwfoTe7nT7Yd2aWpucXTnZB9uqMEqvrPx709mNvPa3UhSCciaywKu9QPA3Qw4mW5tzO6c644co2eSCMiogoy__Qbd-CDnwRFW5GaDVPFOvd5QOPsZgmnszlMipXTm1K3-1m-EXf9q_R3_XmQG6A75aZ8b_SMkPy6urnegdoWqzXQ</recordid><startdate>202111</startdate><enddate>202111</enddate><creator>Wu, Hanqiang</creator><creator>Liang, Jianrong</creator><general>John Wiley & Sons, Inc</general><general>John Wiley and Sons Inc</general><scope>24P</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QP</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>P64</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-3161-4318</orcidid></search><sort><creationdate>202111</creationdate><title>Contributions of NFKB1 ‐94insertion/deletion ATTG polymorphism to the susceptibility of gastrointestinal cancers: A meta‐analysis</title><author>Wu, Hanqiang ; Liang, Jianrong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4484-a102fbcd1943a3436aef373237d2158542d3e0089401f870ed4ce4c55cd7c4023</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Alleles</topic><topic>Cancer</topic><topic>Colorectal cancer</topic><topic>Esophageal cancer</topic><topic>Esophagus</topic><topic>Ethnicity</topic><topic>Gastric cancer</topic><topic>Gastrointestinal cancer</topic><topic>gastrointestinal cancers</topic><topic>Gastrointestinal Neoplasms - diagnosis</topic><topic>Gastrointestinal Neoplasms - epidemiology</topic><topic>Gastrointestinal Neoplasms - etiology</topic><topic>Gene deletion</topic><topic>Gene polymorphism</topic><topic>Genetic Association Studies</topic><topic>Genetic Predisposition to Disease</topic><topic>Humans</topic><topic>Insertion</topic><topic>Meta-analysis</topic><topic>Mutagenesis, Insertional</topic><topic>NF-kappa B p50 Subunit - genetics</topic><topic>NF‐κB1</topic><topic>Odds Ratio</topic><topic>Original</topic><topic>Polymerase chain reaction</topic><topic>Polymorphism</topic><topic>Polymorphism, Genetic</topic><topic>Publication Bias</topic><topic>Sensitivity analysis</topic><topic>Sequence Deletion</topic><topic>SNPs</topic><topic>Susceptibility</topic><topic>Tumorigenesis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wu, Hanqiang</creatorcontrib><creatorcontrib>Liang, Jianrong</creatorcontrib><collection>Wiley Online Library 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 & Calcified Tissue Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</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>ProQuest Central Basic</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of cellular and molecular medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wu, Hanqiang</au><au>Liang, Jianrong</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Contributions of NFKB1 ‐94insertion/deletion ATTG polymorphism to the susceptibility of gastrointestinal cancers: A meta‐analysis</atitle><jtitle>Journal of cellular and molecular medicine</jtitle><addtitle>J Cell Mol Med</addtitle><date>2021-11</date><risdate>2021</risdate><volume>25</volume><issue>22</issue><spage>10674</spage><epage>10683</epage><pages>10674-10683</pages><issn>1582-1838</issn><issn>1582-4934</issn><eissn>1582-4934</eissn><abstract>Nuclear factor‐kappa B1 (NF‐κB1), a pleiotropic transcription factor, functions as a critical contributor to tumorigenesis. Growing numbers of case‐control studies were carried out to analyse the potential contribution of NF‐κB1 gene variants to gastrointestinal cancer risk, yet remains conflicting conclusions. Therefore, we conducted this most up‐to‐date meta‐analysis to evaluate the relationship between NF‐κB1 gene insertion (I)/deletion (D) polymorphism, namely −94ins/delATTG or rs28362491, and the susceptibility to gastrointestinal cancers. We searched PubMed, EMBASE and MEDLINE databases updated in April 2021 for relevant studies. Meta‐analysis was carried out by software Stata11.0. The quantification of the relationship was determined by computing the combined odds ratios (ORs) and their corresponding 95% confidence intervals (CIs). Sensitivity analysis, the funnel plot and Begg's rank correlation test were also applied. Our findings indicate that −94ins/delATTG polymorphism could not significantly impact the susceptibility to gastrointestinal cancers. Under any five genetic models, −94ins/delATTG polymorphism was not remarkedly linked to the risk of colorectal, gastric and oesophageal cancer, respectively. The significant role of −94ins/delATTG was only observed in some certain subgroups. Findings here suggest that NF‐κB1 gene −94ins/delATTG polymorphism may not predispose to gastrointestinal cancer susceptibility.</abstract><cop>England</cop><pub>John Wiley & Sons, Inc</pub><pmid>34672421</pmid><doi>10.1111/jcmm.17004</doi><tpages>10</tpages><orcidid>https://orcid.org/0000-0002-3161-4318</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Alleles Cancer Colorectal cancer Esophageal cancer Esophagus Ethnicity Gastric cancer Gastrointestinal cancer gastrointestinal cancers Gastrointestinal Neoplasms - diagnosis Gastrointestinal Neoplasms - epidemiology Gastrointestinal Neoplasms - etiology Gene deletion Gene polymorphism Genetic Association Studies Genetic Predisposition to Disease Humans Insertion Meta-analysis Mutagenesis, Insertional NF-kappa B p50 Subunit - genetics NF‐κB1 Odds Ratio Original Polymerase chain reaction Polymorphism Polymorphism, Genetic Publication Bias Sensitivity analysis Sequence Deletion SNPs Susceptibility Tumorigenesis |
| title | Contributions of NFKB1 ‐94insertion/deletion ATTG polymorphism to the susceptibility of gastrointestinal cancers: A meta‐analysis |
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