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An inverse relation between cagA+ strains of Helicobacter pylori infection and risk of esophageal and gastric cardia adenocarcinoma
Gastric colonization with Helicobacter pylori, especially cagA+ strains, is a risk factor for noncardia gastric adenocarcinoma, but its relationship with gastric cardia adenocarcinoma is unclear. Although incidence rates for noncardia gastric adenocarcinoma have declined steadily, paralleling a decl...
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| Published in: | Cancer research (Chicago, Ill.) Ill.), 1998-02, Vol.58 (4), p.588-590 |
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| Main Authors: | , , , , , , , , , , , |
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| container_end_page | 590 |
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| container_title | Cancer research (Chicago, Ill.) |
| container_volume | 58 |
| creator | CHOW, W.-H BLASER, M. J WEST, A. B FRAUMENI, J. F BLOT, W. J GAMMON, M. D VAUGHAN, T. L RISCH, H. A PEREZ-PEREZ, G. I SCHOENBERG, J. B STANFORD, J. L ROTTERDAM, H |
| description | Gastric colonization with Helicobacter pylori, especially cagA+ strains, is a risk factor for noncardia gastric adenocarcinoma, but its relationship with gastric cardia adenocarcinoma is unclear. Although incidence rates for noncardia gastric adenocarcinoma have declined steadily, paralleling a decline in H. pylori prevalence, rates for adenocarcinomas of esophagus and gastric cardia have sharply increased in industrialized countries in recent decades. To clarify the role of H. pylori infection in these tumors with divergent incidence trends, we analyzed serum IgG antibodies to H. pylori and to a recombinant fragment of CagA by antigen-specific ELISA among 129 patients newly diagnosed with esophageal/gastric cardia adenocarcinoma, 67 patients with noncardia gastric adenocarcinoma, and 224 population controls. Cancer risks were estimated by odds ratios (OR) and 95% confidence intervals (CI) using logistic regression models. Infection with cagA+ strains was not significantly related to risk for noncardia gastric cancers (OR, 1.4; CI, 0.7-2.8) but was significantly associated with a reduced risk for esophageal/cardia cancers (OR, 0.4; CI, 0.2-0.8). However, there was little association with cagA- strains of H. pylori for either cancer site (OR, 1.0 and 1.1, respectively). These findings suggest that the effects of H. pylori strains on tumor development vary by anatomical site. Further studies are needed to confirm these results and to assess whether the decreasing prevalence of H. pylori, especially cagA+ strains, may be associated with the rising incidence of esophageal/gastric cardia adenocarcinomas in industrialized countries. |
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J ; WEST, A. B ; FRAUMENI, J. F ; BLOT, W. J ; GAMMON, M. D ; VAUGHAN, T. L ; RISCH, H. A ; PEREZ-PEREZ, G. I ; SCHOENBERG, J. B ; STANFORD, J. L ; ROTTERDAM, H</creator><creatorcontrib>CHOW, W.-H ; BLASER, M. J ; WEST, A. B ; FRAUMENI, J. F ; BLOT, W. J ; GAMMON, M. D ; VAUGHAN, T. L ; RISCH, H. A ; PEREZ-PEREZ, G. I ; SCHOENBERG, J. B ; STANFORD, J. L ; ROTTERDAM, H</creatorcontrib><description>Gastric colonization with Helicobacter pylori, especially cagA+ strains, is a risk factor for noncardia gastric adenocarcinoma, but its relationship with gastric cardia adenocarcinoma is unclear. Although incidence rates for noncardia gastric adenocarcinoma have declined steadily, paralleling a decline in H. pylori prevalence, rates for adenocarcinomas of esophagus and gastric cardia have sharply increased in industrialized countries in recent decades. To clarify the role of H. pylori infection in these tumors with divergent incidence trends, we analyzed serum IgG antibodies to H. pylori and to a recombinant fragment of CagA by antigen-specific ELISA among 129 patients newly diagnosed with esophageal/gastric cardia adenocarcinoma, 67 patients with noncardia gastric adenocarcinoma, and 224 population controls. Cancer risks were estimated by odds ratios (OR) and 95% confidence intervals (CI) using logistic regression models. Infection with cagA+ strains was not significantly related to risk for noncardia gastric cancers (OR, 1.4; CI, 0.7-2.8) but was significantly associated with a reduced risk for esophageal/cardia cancers (OR, 0.4; CI, 0.2-0.8). However, there was little association with cagA- strains of H. pylori for either cancer site (OR, 1.0 and 1.1, respectively). These findings suggest that the effects of H. pylori strains on tumor development vary by anatomical site. Further studies are needed to confirm these results and to assess whether the decreasing prevalence of H. pylori, especially cagA+ strains, may be associated with the rising incidence of esophageal/gastric cardia adenocarcinomas in industrialized countries.</description><identifier>ISSN: 0008-5472</identifier><identifier>EISSN: 1538-7445</identifier><identifier>PMID: 9485003</identifier><identifier>CODEN: CNREA8</identifier><language>eng</language><publisher>Philadelphia, PA: American Association for Cancer Research</publisher><subject>Adenocarcinoma - etiology ; Adult ; Aged ; Antigens, Bacterial ; Bacterial Proteins - genetics ; Biological and medical sciences ; Cardia ; Case-Control Studies ; Esophageal Neoplasms - etiology ; Female ; Gastroenterology. Liver. Pancreas. Abdomen ; Genotype ; Helicobacter Infections - complications ; Helicobacter pylori - genetics ; Humans ; Male ; Medical sciences ; Middle Aged ; Risk ; Stomach Neoplasms - etiology ; Stomach. Duodenum. Small intestine. Colon. Rectum. Anus ; Tumors</subject><ispartof>Cancer research (Chicago, Ill.), 1998-02, Vol.58 (4), p.588-590</ispartof><rights>1998 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,786,790</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=2157315$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9485003$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>CHOW, W.-H</creatorcontrib><creatorcontrib>BLASER, M. J</creatorcontrib><creatorcontrib>WEST, A. B</creatorcontrib><creatorcontrib>FRAUMENI, J. F</creatorcontrib><creatorcontrib>BLOT, W. J</creatorcontrib><creatorcontrib>GAMMON, M. D</creatorcontrib><creatorcontrib>VAUGHAN, T. L</creatorcontrib><creatorcontrib>RISCH, H. A</creatorcontrib><creatorcontrib>PEREZ-PEREZ, G. I</creatorcontrib><creatorcontrib>SCHOENBERG, J. B</creatorcontrib><creatorcontrib>STANFORD, J. L</creatorcontrib><creatorcontrib>ROTTERDAM, H</creatorcontrib><title>An inverse relation between cagA+ strains of Helicobacter pylori infection and risk of esophageal and gastric cardia adenocarcinoma</title><title>Cancer research (Chicago, Ill.)</title><addtitle>Cancer Res</addtitle><description>Gastric colonization with Helicobacter pylori, especially cagA+ strains, is a risk factor for noncardia gastric adenocarcinoma, but its relationship with gastric cardia adenocarcinoma is unclear. Although incidence rates for noncardia gastric adenocarcinoma have declined steadily, paralleling a decline in H. pylori prevalence, rates for adenocarcinomas of esophagus and gastric cardia have sharply increased in industrialized countries in recent decades. To clarify the role of H. pylori infection in these tumors with divergent incidence trends, we analyzed serum IgG antibodies to H. pylori and to a recombinant fragment of CagA by antigen-specific ELISA among 129 patients newly diagnosed with esophageal/gastric cardia adenocarcinoma, 67 patients with noncardia gastric adenocarcinoma, and 224 population controls. Cancer risks were estimated by odds ratios (OR) and 95% confidence intervals (CI) using logistic regression models. Infection with cagA+ strains was not significantly related to risk for noncardia gastric cancers (OR, 1.4; CI, 0.7-2.8) but was significantly associated with a reduced risk for esophageal/cardia cancers (OR, 0.4; CI, 0.2-0.8). However, there was little association with cagA- strains of H. pylori for either cancer site (OR, 1.0 and 1.1, respectively). These findings suggest that the effects of H. pylori strains on tumor development vary by anatomical site. Further studies are needed to confirm these results and to assess whether the decreasing prevalence of H. pylori, especially cagA+ strains, may be associated with the rising incidence of esophageal/gastric cardia adenocarcinomas in industrialized countries.</description><subject>Adenocarcinoma - etiology</subject><subject>Adult</subject><subject>Aged</subject><subject>Antigens, Bacterial</subject><subject>Bacterial Proteins - genetics</subject><subject>Biological and medical sciences</subject><subject>Cardia</subject><subject>Case-Control Studies</subject><subject>Esophageal Neoplasms - etiology</subject><subject>Female</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>Genotype</subject><subject>Helicobacter Infections - complications</subject><subject>Helicobacter pylori - genetics</subject><subject>Humans</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Risk</subject><subject>Stomach Neoplasms - etiology</subject><subject>Stomach. Duodenum. Small intestine. Colon. Rectum. 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B</creator><creator>STANFORD, J. L</creator><creator>ROTTERDAM, H</creator><general>American Association for Cancer Research</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope></search><sort><creationdate>19980215</creationdate><title>An inverse relation between cagA+ strains of Helicobacter pylori infection and risk of esophageal and gastric cardia adenocarcinoma</title><author>CHOW, W.-H ; BLASER, M. J ; WEST, A. B ; FRAUMENI, J. F ; BLOT, W. J ; GAMMON, M. D ; VAUGHAN, T. L ; RISCH, H. A ; PEREZ-PEREZ, G. I ; SCHOENBERG, J. B ; STANFORD, J. L ; ROTTERDAM, H</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-h269t-2c9fa4348d8d74b27f3fcd103b84c5b4f8303980350672e52ce0bd28b83c852c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1998</creationdate><topic>Adenocarcinoma - etiology</topic><topic>Adult</topic><topic>Aged</topic><topic>Antigens, Bacterial</topic><topic>Bacterial Proteins - genetics</topic><topic>Biological and medical sciences</topic><topic>Cardia</topic><topic>Case-Control Studies</topic><topic>Esophageal Neoplasms - etiology</topic><topic>Female</topic><topic>Gastroenterology. Liver. Pancreas. Abdomen</topic><topic>Genotype</topic><topic>Helicobacter Infections - complications</topic><topic>Helicobacter pylori - genetics</topic><topic>Humans</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Risk</topic><topic>Stomach Neoplasms - etiology</topic><topic>Stomach. Duodenum. Small intestine. Colon. Rectum. Anus</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>CHOW, W.-H</creatorcontrib><creatorcontrib>BLASER, M. J</creatorcontrib><creatorcontrib>WEST, A. B</creatorcontrib><creatorcontrib>FRAUMENI, J. F</creatorcontrib><creatorcontrib>BLOT, W. J</creatorcontrib><creatorcontrib>GAMMON, M. D</creatorcontrib><creatorcontrib>VAUGHAN, T. L</creatorcontrib><creatorcontrib>RISCH, H. A</creatorcontrib><creatorcontrib>PEREZ-PEREZ, G. I</creatorcontrib><creatorcontrib>SCHOENBERG, J. B</creatorcontrib><creatorcontrib>STANFORD, J. L</creatorcontrib><creatorcontrib>ROTTERDAM, H</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><jtitle>Cancer research (Chicago, Ill.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>CHOW, W.-H</au><au>BLASER, M. J</au><au>WEST, A. B</au><au>FRAUMENI, J. F</au><au>BLOT, W. J</au><au>GAMMON, M. D</au><au>VAUGHAN, T. L</au><au>RISCH, H. A</au><au>PEREZ-PEREZ, G. I</au><au>SCHOENBERG, J. B</au><au>STANFORD, J. L</au><au>ROTTERDAM, H</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>An inverse relation between cagA+ strains of Helicobacter pylori infection and risk of esophageal and gastric cardia adenocarcinoma</atitle><jtitle>Cancer research (Chicago, Ill.)</jtitle><addtitle>Cancer Res</addtitle><date>1998-02-15</date><risdate>1998</risdate><volume>58</volume><issue>4</issue><spage>588</spage><epage>590</epage><pages>588-590</pages><issn>0008-5472</issn><eissn>1538-7445</eissn><coden>CNREA8</coden><notes>ObjectType-Article-1</notes><notes>SourceType-Scholarly Journals-1</notes><notes>ObjectType-Feature-2</notes><notes>content type line 23</notes><abstract>Gastric colonization with Helicobacter pylori, especially cagA+ strains, is a risk factor for noncardia gastric adenocarcinoma, but its relationship with gastric cardia adenocarcinoma is unclear. Although incidence rates for noncardia gastric adenocarcinoma have declined steadily, paralleling a decline in H. pylori prevalence, rates for adenocarcinomas of esophagus and gastric cardia have sharply increased in industrialized countries in recent decades. To clarify the role of H. pylori infection in these tumors with divergent incidence trends, we analyzed serum IgG antibodies to H. pylori and to a recombinant fragment of CagA by antigen-specific ELISA among 129 patients newly diagnosed with esophageal/gastric cardia adenocarcinoma, 67 patients with noncardia gastric adenocarcinoma, and 224 population controls. Cancer risks were estimated by odds ratios (OR) and 95% confidence intervals (CI) using logistic regression models. Infection with cagA+ strains was not significantly related to risk for noncardia gastric cancers (OR, 1.4; CI, 0.7-2.8) but was significantly associated with a reduced risk for esophageal/cardia cancers (OR, 0.4; CI, 0.2-0.8). However, there was little association with cagA- strains of H. pylori for either cancer site (OR, 1.0 and 1.1, respectively). These findings suggest that the effects of H. pylori strains on tumor development vary by anatomical site. Further studies are needed to confirm these results and to assess whether the decreasing prevalence of H. pylori, especially cagA+ strains, may be associated with the rising incidence of esophageal/gastric cardia adenocarcinomas in industrialized countries.</abstract><cop>Philadelphia, PA</cop><pub>American Association for Cancer Research</pub><pmid>9485003</pmid><tpages>3</tpages></addata></record> |
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| ispartof | Cancer research (Chicago, Ill.), 1998-02, Vol.58 (4), p.588-590 |
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| language | eng |
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| subjects | Adenocarcinoma - etiology Adult Aged Antigens, Bacterial Bacterial Proteins - genetics Biological and medical sciences Cardia Case-Control Studies Esophageal Neoplasms - etiology Female Gastroenterology. Liver. Pancreas. Abdomen Genotype Helicobacter Infections - complications Helicobacter pylori - genetics Humans Male Medical sciences Middle Aged Risk Stomach Neoplasms - etiology Stomach. Duodenum. Small intestine. Colon. Rectum. Anus Tumors |
| title | An inverse relation between cagA+ strains of Helicobacter pylori infection and risk of esophageal and gastric cardia adenocarcinoma |
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