Viruses, Other Pathogenic Microorganisms and Esophageal Cancer
Identifieur interne : 000015 ( Pmc/Corpus ); précédent : 000014; suivant : 000016Viruses, Other Pathogenic Microorganisms and Esophageal Cancer
Auteurs : Wenjia Xu ; Zhongshun Liu ; Qunchao Bao ; Zhikang QianSource :
- Gastrointestinal Tumors [ 2296-3774 ] ; 2015.
Abstract
Esophageal cancer (EC) is the eighth most prevalent malignant tumor and the sixth leading cause of cancer mortality throughout the world. Despite the technical developments in diagnosis and treatment, the 5-year survival rate is still low. The etiology of EC remains poorly understood; multiple risk factors may be involved and account for the great variation in EC incidence in different geographic regions.
Infection with carcinogenetic pathogens has been proposed as a risk factor for EC. This review explores the recent studies on the association of human papillomavirus (HPV), Epstein-Barr virus (EBV),
Among the above-mentioned pathogens, HPV most likely contributes to esophageal squamous cell carcinoma (ESCC) in high-risk populations. New techniques are being applied to studies on the role of infection in EC, which will inevitably bring novel ideas to the field in the near future.
Multiple meta-analyses support the finding of a higher HPV detection rate in regions associated with high risk for ESCC compared to low-risk areas. A potential role of HPV in the rise of esophageal adenocarcinoma (EAC) was proposed recently. However, further studies are required before a firm conclusion can be drawn. Less work has been done in studying the association between EBV and ESCC, and the results are quite controversial.
Url:
DOI: 10.1159/000380897
PubMed: 26674173
PubMed Central: 4668794
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Viruses, Other Pathogenic Microorganisms and Esophageal Cancer</title><author><name sortKey="Xu, Wenjia" sort="Xu, Wenjia" uniqKey="Xu W" first="Wenjia" last="Xu">Wenjia Xu</name></author><author><name sortKey="Liu, Zhongshun" sort="Liu, Zhongshun" uniqKey="Liu Z" first="Zhongshun" last="Liu">Zhongshun Liu</name></author><author><name sortKey="Bao, Qunchao" sort="Bao, Qunchao" uniqKey="Bao Q" first="Qunchao" last="Bao">Qunchao Bao</name></author><author><name sortKey="Qian, Zhikang" sort="Qian, Zhikang" uniqKey="Qian Z" first="Zhikang" last="Qian">Zhikang Qian</name></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">26674173</idno><idno type="pmc">4668794</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4668794</idno><idno type="RBID">PMC:4668794</idno><idno type="doi">10.1159/000380897</idno><date when="2015">2015</date><idno type="wicri:Area/Pmc/Corpus">000015</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000015</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Viruses, Other Pathogenic Microorganisms and Esophageal Cancer</title><author><name sortKey="Xu, Wenjia" sort="Xu, Wenjia" uniqKey="Xu W" first="Wenjia" last="Xu">Wenjia Xu</name></author><author><name sortKey="Liu, Zhongshun" sort="Liu, Zhongshun" uniqKey="Liu Z" first="Zhongshun" last="Liu">Zhongshun Liu</name></author><author><name sortKey="Bao, Qunchao" sort="Bao, Qunchao" uniqKey="Bao Q" first="Qunchao" last="Bao">Qunchao Bao</name></author><author><name sortKey="Qian, Zhikang" sort="Qian, Zhikang" uniqKey="Qian Z" first="Zhikang" last="Qian">Zhikang Qian</name></author></analytic><series><title level="j">Gastrointestinal Tumors</title><idno type="ISSN">2296-3774</idno><idno type="eISSN">2296-3766</idno><imprint><date when="2015">2015</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><sec><title>Background</title><p>Esophageal cancer (EC) is the eighth most prevalent malignant tumor and the sixth leading cause of cancer mortality throughout the world. Despite the technical developments in diagnosis and treatment, the 5-year survival rate is still low. The etiology of EC remains poorly understood; multiple risk factors may be involved and account for the great variation in EC incidence in different geographic regions.</p></sec><sec><title>Summary</title><p>Infection with carcinogenetic pathogens has been proposed as a risk factor for EC. This review explores the recent studies on the association of human papillomavirus (HPV), Epstein-Barr virus (EBV), <italic>Helicobacter pylori</italic> and esophageal bacterial biota with EC.</p></sec><sec><title>Key Message</title><p>Among the above-mentioned pathogens, HPV most likely contributes to esophageal squamous cell carcinoma (ESCC) in high-risk populations. New techniques are being applied to studies on the role of infection in EC, which will inevitably bring novel ideas to the field in the near future.</p></sec><sec><title>Practical Implications</title><p>Multiple meta-analyses support the finding of a higher HPV detection rate in regions associated with high risk for ESCC compared to low-risk areas. A potential role of HPV in the rise of esophageal adenocarcinoma (EAC) was proposed recently. However, further studies are required before a firm conclusion can be drawn. Less work has been done in studying the association between EBV and ESCC, and the results are quite controversial. <italic>H. pylori</italic> infection is found to be inversely related to EC, which is probably due to the reduced incidence of gastroesophageal reflux disease. Analysis of the esophageal bacterial biota revealed distinct clusters of bacteria in normal and diseased esophagi. A type II microbiome rich in Gram-negative bacteria potentially contributes to EAC by inducing chronic inflammation. Novel findings from such studies as these may benefit public health by justifying anti-infection measures to prevent EC.</p></sec></div></front></TEI><pmc article-type="review-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<front><journal-meta><journal-id journal-id-type="nlm-ta">Gastrointest Tumors</journal-id><journal-id journal-id-type="iso-abbrev">Gastrointest Tumors</journal-id><journal-id journal-id-type="publisher-id">GAT</journal-id><journal-title-group><journal-title>Gastrointestinal Tumors</journal-title></journal-title-group><issn pub-type="ppub">2296-3774</issn><issn pub-type="epub">2296-3766</issn><publisher><publisher-name>S. Karger AG</publisher-name><publisher-loc>Allschwilerstrasse 10, P.O. Box · Postfach · Case postale, CH–4009, Basel, Switzerland · Schweiz · Suisse, Phone: +41 61 306 11 11, Fax: +41 61 306 12 34, karger@karger.ch</publisher-loc></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">26674173</article-id><article-id pub-id-type="pmc">4668794</article-id><article-id pub-id-type="doi">10.1159/000380897</article-id><article-id pub-id-type="publisher-id">gat-0002-0002</article-id><article-categories><subj-group subj-group-type="heading"><subject>Mini-Review</subject></subj-group></article-categories><title-group><article-title>Viruses, Other Pathogenic Microorganisms and Esophageal Cancer</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Xu</surname><given-names>Wenjia</given-names></name></contrib><contrib contrib-type="author"><name><surname>Liu</surname><given-names>Zhongshun</given-names></name></contrib><contrib contrib-type="author"><name><surname>Bao</surname><given-names>Qunchao</given-names></name></contrib><contrib contrib-type="author"><name><surname>Qian</surname><given-names>Zhikang</given-names></name><xref ref-type="corresp" rid="cor1">*</xref></contrib></contrib-group><aff>Unit of Herpesvirus and Molecular Virology, Key Laboratory of Molecular Virology & Immunology, Institut Pasteur of Shanghai, Chinese Academy of Sciences, Shanghai, China</aff><author-notes><corresp id="cor1">*Zhikang Qian, Key Laboratory of Molecular Virology & Immunology, Institut Pasteur of Shanghai Chinese Academy of Sciences, Life Science Research Building, 320 Yueyang Road, Xuhui District, Shanghai 200031 (China), E-Mail <email>zkqian@ips.ac.cn</email></corresp></author-notes><pub-date pub-type="ppub"><month>5</month><year>2015</year></pub-date><pub-date pub-type="epub"><day>8</day><month>4</month><year>2015</year></pub-date><pub-date pub-type="pmc-release"><day>8</day><month>4</month><year>2015</year></pub-date><pmc-comment> PMC Release delay is 0 months and 0 days and was based on the
<volume>2</volume><issue>1</issue><fpage>2</fpage><lpage>13</lpage><permissions><copyright-statement>Copyright © 2015 by S. Karger AG, Basel</copyright-statement><copyright-year>2015</copyright-year></permissions><abstract><sec><title>Background</title><p>Esophageal cancer (EC) is the eighth most prevalent malignant tumor and the sixth leading cause of cancer mortality throughout the world. Despite the technical developments in diagnosis and treatment, the 5-year survival rate is still low. The etiology of EC remains poorly understood; multiple risk factors may be involved and account for the great variation in EC incidence in different geographic regions.</p></sec><sec><title>Summary</title><p>Infection with carcinogenetic pathogens has been proposed as a risk factor for EC. This review explores the recent studies on the association of human papillomavirus (HPV), Epstein-Barr virus (EBV), <italic>Helicobacter pylori</italic> and esophageal bacterial biota with EC.</p></sec><sec><title>Key Message</title><p>Among the above-mentioned pathogens, HPV most likely contributes to esophageal squamous cell carcinoma (ESCC) in high-risk populations. New techniques are being applied to studies on the role of infection in EC, which will inevitably bring novel ideas to the field in the near future.</p></sec><sec><title>Practical Implications</title><p>Multiple meta-analyses support the finding of a higher HPV detection rate in regions associated with high risk for ESCC compared to low-risk areas. A potential role of HPV in the rise of esophageal adenocarcinoma (EAC) was proposed recently. However, further studies are required before a firm conclusion can be drawn. Less work has been done in studying the association between EBV and ESCC, and the results are quite controversial. <italic>H. pylori</italic> infection is found to be inversely related to EC, which is probably due to the reduced incidence of gastroesophageal reflux disease. Analysis of the esophageal bacterial biota revealed distinct clusters of bacteria in normal and diseased esophagi. A type II microbiome rich in Gram-negative bacteria potentially contributes to EAC by inducing chronic inflammation. Novel findings from such studies as these may benefit public health by justifying anti-infection measures to prevent EC.</p></sec></abstract><kwd-group><title>Key Words</title><kwd>Bacterial biota</kwd><kwd>Epstein-Barr virus</kwd><kwd>Esophageal cancer</kwd><kwd>Esophageal squamous cell carcinoma</kwd><kwd>Human papillomavirus</kwd></kwd-group><counts><table-count count="2"></table-count><ref-count count="80"></ref-count><page-count count="12"></page-count></counts></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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