Precancerous Gastric Lesions with Helicobacter pylori vacA+/babA2+/oipA+ Genotype Increase the Risk of Gastric Cancer
Objective. The clinical outcomes of gastric diseases such as chronic gastritis, peptic ulcer, and gastric cancer have been attributed to the interplay of virulence factors of Helicobacter pylori (H. pylori), host genetic susceptibility, and host immune responses. This study investigated the presence...
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| description | Objective. The clinical outcomes of gastric diseases such as chronic gastritis, peptic ulcer, and gastric cancer have been attributed to the interplay of virulence factors of Helicobacter pylori (H. pylori), host genetic susceptibility, and host immune responses. This study investigated the presence of cagA, vacA, iceA2, babA2, and oipA genes and their association with clinical outcomes. Methods. Chronic gastritis, atrophic gastritis, and intestinal metaplasia specimens were obtained from patients who underwent endoscopy and surgical resection between January 2017 and December 2018; specimens from gastric cancer patients treated between January 2014 and December 2018 were also added. H. pylori infection and virulence genes (cagA, vacA, iceA2, babA2, and oipA) were determined using real-time PCR. The association between H. pylori genotypes and clinical outcomes were evaluated using multivariate regression model analysis. The overall survival of gastric cancer patients was compared between genotype combinations. Results. H. pylori was positive in 166 patients with chronic gastritis, precancerous gastric lesions, and gastric cancer. The genes vacA, babA2, and oipA were most prevalent in chronic gastritis (73%), precancerous gastric lesions (62%), and gastric cancer (91%), respectively. The vacA, babA2, and oipA genes were associated with increased risk of gastric cancer (OR = 1.23; 95% CI = 1.13–3.32; P=0.033, OR = 2.64; 95% CI = 1.44–4.82, P=0.024, and OR = 2.79; 95% CI = 1.58–5.41; P=0.031, respectively). Interestingly, H. pylori vacA+/babA2+/oipA+ genotype infection was associated with increased risk of gastric cancer (OR = 3.85, 95% CI = 1.67–5.77, P=0.014). Conclusion. In this present study, we reported on the virulence genes of H. pylori infection to reveal their association with increased risk of chronic gastritis, precancerous gastric lesions, and gastric cancer. Precancerous gastric lesions with H. pylori vacA+/babA2+/oipA+ genotype increased the risk of gastric cancer. |
| doi_str_mv | 10.1155/2020/7243029 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_7049835</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2375502260</sourcerecordid><originalsourceid>FETCH-LOGICAL-e298t-4c35fd90874996a09f587f374e741ece06c02932b249b5f42d50b72a7b4b7eb23</originalsourceid><addsrcrecordid>eNpdkU1rGzEQhkVpaEKSW89F0EvBuNa3VpeCMa0TMLSU9iwkebZWul5tpd0E__sqtXFp5zID8_DOx4vQa0reUyrlghFGFpoJTph5ga4Yp2KuqKAvzzXnl-i2lAdSo6GKGPUKXXJGhaHMXKHpS4bg-gA5TQWvXRlzDHgDJaa-4Kc47vAddDEk78IIGQ-HLuWIH11Yzhbe-SWbLVIcljO8hj6NhwHwfR8yuAJ43AH-GstPnNqz8urPrBt00bquwO0pX6Pvnz5-W93NN5_X96vlZg7MNONcBC7brSGNFsYoR0wrG91yLUALCgGICvVuzjwTxstWsK0kXjOnvfAaPOPX6MNRd5j8HrYB-jG7zg457l0-2OSi_bfTx539kR6tJsI0XFaBdyeBnH5NUEa7jyVA17ke6sMs41pKwpgiFX37H_qQptzX8yqlDCNcG16p2ZHaxX7rnuJ5F0rss6P22VF7crTSb440VAZa95emXClN-W9WCJo3</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2369203793</pqid></control><display><type>article</type><title>Precancerous Gastric Lesions with Helicobacter pylori vacA+/babA2+/oipA+ Genotype Increase the Risk of Gastric Cancer</title><source>Wiley Online Library Open Access</source><source>PubMed Central</source><source>Alma/SFX Local Collection</source><source>PubMed Central Open Access</source><creator>Kangwantas, Kokiet ; Paoin, Chatchanok ; Tongtawee, Taweesak ; Wattanawongdon, Wareeporn ; Bartpho, Theeraya Simawaranon ; Dechsukhum, Chavaboon</creator><contributor>Tong, Qiang</contributor><creatorcontrib>Kangwantas, Kokiet ; Paoin, Chatchanok ; Tongtawee, Taweesak ; Wattanawongdon, Wareeporn ; Bartpho, Theeraya Simawaranon ; Dechsukhum, Chavaboon ; Tong, Qiang</creatorcontrib><description>Objective. The clinical outcomes of gastric diseases such as chronic gastritis, peptic ulcer, and gastric cancer have been attributed to the interplay of virulence factors of Helicobacter pylori (H. pylori), host genetic susceptibility, and host immune responses. This study investigated the presence of cagA, vacA, iceA2, babA2, and oipA genes and their association with clinical outcomes. Methods. Chronic gastritis, atrophic gastritis, and intestinal metaplasia specimens were obtained from patients who underwent endoscopy and surgical resection between January 2017 and December 2018; specimens from gastric cancer patients treated between January 2014 and December 2018 were also added. H. pylori infection and virulence genes (cagA, vacA, iceA2, babA2, and oipA) were determined using real-time PCR. The association between H. pylori genotypes and clinical outcomes were evaluated using multivariate regression model analysis. The overall survival of gastric cancer patients was compared between genotype combinations. Results. H. pylori was positive in 166 patients with chronic gastritis, precancerous gastric lesions, and gastric cancer. The genes vacA, babA2, and oipA were most prevalent in chronic gastritis (73%), precancerous gastric lesions (62%), and gastric cancer (91%), respectively. The vacA, babA2, and oipA genes were associated with increased risk of gastric cancer (OR = 1.23; 95% CI = 1.13–3.32; P=0.033, OR = 2.64; 95% CI = 1.44–4.82, P=0.024, and OR = 2.79; 95% CI = 1.58–5.41; P=0.031, respectively). Interestingly, H. pylori vacA+/babA2+/oipA+ genotype infection was associated with increased risk of gastric cancer (OR = 3.85, 95% CI = 1.67–5.77, P=0.014). Conclusion. In this present study, we reported on the virulence genes of H. pylori infection to reveal their association with increased risk of chronic gastritis, precancerous gastric lesions, and gastric cancer. Precancerous gastric lesions with H. pylori vacA+/babA2+/oipA+ genotype increased the risk of gastric cancer.</description><identifier>ISSN: 2314-6133</identifier><identifier>EISSN: 2314-6141</identifier><identifier>DOI: 10.1155/2020/7243029</identifier><identifier>PMID: 32149129</identifier><language>eng</language><publisher>Cairo, Egypt: Hindawi Publishing Corporation</publisher><subject>Biopsy ; Cancer ; Chronic infection ; Clinical outcomes ; Deoxyribonucleic acid ; DNA ; Endoscopy ; Gastric cancer ; Gastritis ; Genes ; Genetic engineering ; Genotype & phenotype ; Genotypes ; Health risks ; Helicobacter pylori ; Hospitals ; Immune response ; Infections ; Intestine ; Lesions ; Metaplasia ; Patients ; Peptic ulcers ; Proteins ; Regression analysis ; Regression models ; Risk ; Survival analysis ; Virulence ; Virulence factors</subject><ispartof>BioMed research international, 2020-01, Vol.2020 (2020), p.1-8</ispartof><rights>Copyright © 2020 Theeraya Simawaranon Bartpho et al.</rights><rights>Copyright © 2020 Theeraya Simawaranon Bartpho et al. This is an open access article distributed under the Creative Commons Attribution License (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. http://creativecommons.org/licenses/by/4.0</rights><rights>Copyright © 2020 Theeraya Simawaranon Bartpho et al. 2020</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><orcidid>0000-0002-1976-9878</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/PMC7049835/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7049835/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids></links><search><contributor>Tong, Qiang</contributor><creatorcontrib>Kangwantas, Kokiet</creatorcontrib><creatorcontrib>Paoin, Chatchanok</creatorcontrib><creatorcontrib>Tongtawee, Taweesak</creatorcontrib><creatorcontrib>Wattanawongdon, Wareeporn</creatorcontrib><creatorcontrib>Bartpho, Theeraya Simawaranon</creatorcontrib><creatorcontrib>Dechsukhum, Chavaboon</creatorcontrib><title>Precancerous Gastric Lesions with Helicobacter pylori vacA+/babA2+/oipA+ Genotype Increase the Risk of Gastric Cancer</title><title>BioMed research international</title><description>Objective. The clinical outcomes of gastric diseases such as chronic gastritis, peptic ulcer, and gastric cancer have been attributed to the interplay of virulence factors of Helicobacter pylori (H. pylori), host genetic susceptibility, and host immune responses. This study investigated the presence of cagA, vacA, iceA2, babA2, and oipA genes and their association with clinical outcomes. Methods. Chronic gastritis, atrophic gastritis, and intestinal metaplasia specimens were obtained from patients who underwent endoscopy and surgical resection between January 2017 and December 2018; specimens from gastric cancer patients treated between January 2014 and December 2018 were also added. H. pylori infection and virulence genes (cagA, vacA, iceA2, babA2, and oipA) were determined using real-time PCR. The association between H. pylori genotypes and clinical outcomes were evaluated using multivariate regression model analysis. The overall survival of gastric cancer patients was compared between genotype combinations. Results. H. pylori was positive in 166 patients with chronic gastritis, precancerous gastric lesions, and gastric cancer. The genes vacA, babA2, and oipA were most prevalent in chronic gastritis (73%), precancerous gastric lesions (62%), and gastric cancer (91%), respectively. The vacA, babA2, and oipA genes were associated with increased risk of gastric cancer (OR = 1.23; 95% CI = 1.13–3.32; P=0.033, OR = 2.64; 95% CI = 1.44–4.82, P=0.024, and OR = 2.79; 95% CI = 1.58–5.41; P=0.031, respectively). Interestingly, H. pylori vacA+/babA2+/oipA+ genotype infection was associated with increased risk of gastric cancer (OR = 3.85, 95% CI = 1.67–5.77, P=0.014). Conclusion. In this present study, we reported on the virulence genes of H. pylori infection to reveal their association with increased risk of chronic gastritis, precancerous gastric lesions, and gastric cancer. Precancerous gastric lesions with H. pylori vacA+/babA2+/oipA+ genotype increased the risk of gastric cancer.</description><subject>Biopsy</subject><subject>Cancer</subject><subject>Chronic infection</subject><subject>Clinical outcomes</subject><subject>Deoxyribonucleic acid</subject><subject>DNA</subject><subject>Endoscopy</subject><subject>Gastric cancer</subject><subject>Gastritis</subject><subject>Genes</subject><subject>Genetic engineering</subject><subject>Genotype & phenotype</subject><subject>Genotypes</subject><subject>Health risks</subject><subject>Helicobacter pylori</subject><subject>Hospitals</subject><subject>Immune response</subject><subject>Infections</subject><subject>Intestine</subject><subject>Lesions</subject><subject>Metaplasia</subject><subject>Patients</subject><subject>Peptic ulcers</subject><subject>Proteins</subject><subject>Regression analysis</subject><subject>Regression models</subject><subject>Risk</subject><subject>Survival analysis</subject><subject>Virulence</subject><subject>Virulence factors</subject><issn>2314-6133</issn><issn>2314-6141</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>RHX</sourceid><sourceid>BENPR</sourceid><recordid>eNpdkU1rGzEQhkVpaEKSW89F0EvBuNa3VpeCMa0TMLSU9iwkebZWul5tpd0E__sqtXFp5zID8_DOx4vQa0reUyrlghFGFpoJTph5ga4Yp2KuqKAvzzXnl-i2lAdSo6GKGPUKXXJGhaHMXKHpS4bg-gA5TQWvXRlzDHgDJaa-4Kc47vAddDEk78IIGQ-HLuWIH11Yzhbe-SWbLVIcljO8hj6NhwHwfR8yuAJ43AH-GstPnNqz8urPrBt00bquwO0pX6Pvnz5-W93NN5_X96vlZg7MNONcBC7brSGNFsYoR0wrG91yLUALCgGICvVuzjwTxstWsK0kXjOnvfAaPOPX6MNRd5j8HrYB-jG7zg457l0-2OSi_bfTx539kR6tJsI0XFaBdyeBnH5NUEa7jyVA17ke6sMs41pKwpgiFX37H_qQptzX8yqlDCNcG16p2ZHaxX7rnuJ5F0rss6P22VF7crTSb440VAZa95emXClN-W9WCJo3</recordid><startdate>20200101</startdate><enddate>20200101</enddate><creator>Kangwantas, Kokiet</creator><creator>Paoin, Chatchanok</creator><creator>Tongtawee, Taweesak</creator><creator>Wattanawongdon, Wareeporn</creator><creator>Bartpho, Theeraya Simawaranon</creator><creator>Dechsukhum, Chavaboon</creator><general>Hindawi Publishing Corporation</general><general>Hindawi</general><general>Hindawi 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Gastric Lesions with Helicobacter pylori vacA+/babA2+/oipA+ Genotype Increase the Risk of Gastric Cancer</title><author>Kangwantas, Kokiet ; Paoin, Chatchanok ; Tongtawee, Taweesak ; Wattanawongdon, Wareeporn ; Bartpho, Theeraya Simawaranon ; Dechsukhum, Chavaboon</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-e298t-4c35fd90874996a09f587f374e741ece06c02932b249b5f42d50b72a7b4b7eb23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Biopsy</topic><topic>Cancer</topic><topic>Chronic infection</topic><topic>Clinical outcomes</topic><topic>Deoxyribonucleic acid</topic><topic>DNA</topic><topic>Endoscopy</topic><topic>Gastric cancer</topic><topic>Gastritis</topic><topic>Genes</topic><topic>Genetic engineering</topic><topic>Genotype & phenotype</topic><topic>Genotypes</topic><topic>Health risks</topic><topic>Helicobacter pylori</topic><topic>Hospitals</topic><topic>Immune response</topic><topic>Infections</topic><topic>Intestine</topic><topic>Lesions</topic><topic>Metaplasia</topic><topic>Patients</topic><topic>Peptic ulcers</topic><topic>Proteins</topic><topic>Regression analysis</topic><topic>Regression models</topic><topic>Risk</topic><topic>Survival analysis</topic><topic>Virulence</topic><topic>Virulence factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kangwantas, Kokiet</creatorcontrib><creatorcontrib>Paoin, Chatchanok</creatorcontrib><creatorcontrib>Tongtawee, Taweesak</creatorcontrib><creatorcontrib>Wattanawongdon, Wareeporn</creatorcontrib><creatorcontrib>Bartpho, Theeraya Simawaranon</creatorcontrib><creatorcontrib>Dechsukhum, Chavaboon</creatorcontrib><collection>الدوريات العلمية والإحصائية - e-Marefa Academic and Statistical Periodicals</collection><collection>معرفة - المحتوى العربي الأكاديمي المتكامل - e-Marefa Academic Complete</collection><collection>Hindawi Publishing 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Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>BioMed research international</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kangwantas, Kokiet</au><au>Paoin, Chatchanok</au><au>Tongtawee, Taweesak</au><au>Wattanawongdon, Wareeporn</au><au>Bartpho, Theeraya Simawaranon</au><au>Dechsukhum, Chavaboon</au><au>Tong, Qiang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Precancerous Gastric Lesions with Helicobacter pylori vacA+/babA2+/oipA+ Genotype Increase the Risk of Gastric Cancer</atitle><jtitle>BioMed research international</jtitle><date>2020-01-01</date><risdate>2020</risdate><volume>2020</volume><issue>2020</issue><spage>1</spage><epage>8</epage><pages>1-8</pages><issn>2314-6133</issn><eissn>2314-6141</eissn><abstract>Objective. The clinical outcomes of gastric diseases such as chronic gastritis, peptic ulcer, and gastric cancer have been attributed to the interplay of virulence factors of Helicobacter pylori (H. pylori), host genetic susceptibility, and host immune responses. This study investigated the presence of cagA, vacA, iceA2, babA2, and oipA genes and their association with clinical outcomes. Methods. Chronic gastritis, atrophic gastritis, and intestinal metaplasia specimens were obtained from patients who underwent endoscopy and surgical resection between January 2017 and December 2018; specimens from gastric cancer patients treated between January 2014 and December 2018 were also added. H. pylori infection and virulence genes (cagA, vacA, iceA2, babA2, and oipA) were determined using real-time PCR. The association between H. pylori genotypes and clinical outcomes were evaluated using multivariate regression model analysis. The overall survival of gastric cancer patients was compared between genotype combinations. Results. H. pylori was positive in 166 patients with chronic gastritis, precancerous gastric lesions, and gastric cancer. The genes vacA, babA2, and oipA were most prevalent in chronic gastritis (73%), precancerous gastric lesions (62%), and gastric cancer (91%), respectively. The vacA, babA2, and oipA genes were associated with increased risk of gastric cancer (OR = 1.23; 95% CI = 1.13–3.32; P=0.033, OR = 2.64; 95% CI = 1.44–4.82, P=0.024, and OR = 2.79; 95% CI = 1.58–5.41; P=0.031, respectively). Interestingly, H. pylori vacA+/babA2+/oipA+ genotype infection was associated with increased risk of gastric cancer (OR = 3.85, 95% CI = 1.67–5.77, P=0.014). Conclusion. In this present study, we reported on the virulence genes of H. pylori infection to reveal their association with increased risk of chronic gastritis, precancerous gastric lesions, and gastric cancer. Precancerous gastric lesions with H. pylori vacA+/babA2+/oipA+ genotype increased the risk of gastric cancer.</abstract><cop>Cairo, Egypt</cop><pub>Hindawi Publishing Corporation</pub><pmid>32149129</pmid><doi>10.1155/2020/7243029</doi><tpages>8</tpages><orcidid>https://orcid.org/0000-0002-1976-9878</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Biopsy Cancer Chronic infection Clinical outcomes Deoxyribonucleic acid DNA Endoscopy Gastric cancer Gastritis Genes Genetic engineering Genotype & phenotype Genotypes Health risks Helicobacter pylori Hospitals Immune response Infections Intestine Lesions Metaplasia Patients Peptic ulcers Proteins Regression analysis Regression models Risk Survival analysis Virulence Virulence factors |
| title | Precancerous Gastric Lesions with Helicobacter pylori vacA+/babA2+/oipA+ Genotype Increase the Risk of Gastric Cancer |
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