{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,8]],"date-time":"2026-02-08T06:28:01Z","timestamp":1770532081000,"version":"3.49.0"},"reference-count":39,"publisher":"BMJ","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Gut"],"accepted":{"date-parts":[[1998,4,14]]},"published-print":{"date-parts":[[1998,12,1]]},"abstract":"<jats:p>\n                    <jats:italic>Background<\/jats:italic>\n                    \u2014The development of clinical disease after infection with\n                    <jats:italic>Helicobacter pylori<\/jats:italic>\n                    has been reported to be associated with expression of the\n                    <jats:italic>cagA<\/jats:italic>\n                    gene. Recently, it has been shown that\n                    <jats:italic>cagA<\/jats:italic>\n                    is part of a multigene locus, described as the\n                    <jats:italic>cag<\/jats:italic>\n                    pathogenicity island (PAI). The role of this region in determining clinical outcome remains to be established.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:italic>Aims<\/jats:italic>\n                    \u2014To investigate whether the presence of\n                    <jats:italic>cagA<\/jats:italic>\n                    is always associated with the presence of the complete\n                    <jats:italic>cag<\/jats:italic>\n                    PAI and to evaluate the distribution of selected\n                    <jats:italic>cag<\/jats:italic>\n                    genes in 73\n                    <jats:italic>H pylori<\/jats:italic>\n                    strains isolated from patients in France.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:italic>Methods<\/jats:italic>\n                    \u2014Clinical strains of\n                    <jats:italic>H pylori<\/jats:italic>\n                    were screened for selected genes of the\n                    <jats:italic>cag<\/jats:italic>\n                    PAI by polymerase chain reaction and colony hybridisation.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:italic>Results<\/jats:italic>\n                    \u2014Of 64 strains that harboured the\n                    <jats:italic>cagA<\/jats:italic>\n                    gene, 57 (89%) also contained the entire\n                    <jats:italic>cag<\/jats:italic>\n                    PAI. The entire\n                    <jats:italic>cag<\/jats:italic>\n                    PAI was found in 85% (48\/56) and 53% (9\/17) of duodenal ulcer and non-ulcer dyspepsia isolates, respectively. Eight strains had deletions within the\n                    <jats:italic>cag<\/jats:italic>\n                    PAI, including deletion of the\n                    <jats:italic>cagA<\/jats:italic>\n                    gene in one isolate; the deletions were not associated with the insertion sequence IS605. Of eight strains lacking the\n                    <jats:italic>cag<\/jats:italic>\n                    PAI, four were isolated from patients with duodenal ulcer.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:italic>Conclusion<\/jats:italic>\n                    \u2014The\n                    <jats:italic>cag<\/jats:italic>\n                    PAI is not a uniform, conserved entity. Although the presence of the\n                    <jats:italic>cag<\/jats:italic>\n                    PAI is highly associated with duodenal ulcer, the clinical outcome of infection with\n                    <jats:italic>H pylori<\/jats:italic>\n                    is not reliably predicted by any gene of the\n                    <jats:italic>cag<\/jats:italic>\n                    PAI.\n                  <\/jats:p>","DOI":"10.1136\/gut.43.6.752","type":"journal-article","created":{"date-parts":[[2010,6,30]],"date-time":"2010-06-30T12:46:12Z","timestamp":1277901972000},"page":"752-758","source":"Crossref","is-referenced-by-count":91,"title":["Clinical outcome after infection with\n                    <i>Helicobacter pylori<\/i>\n                    does not appear to be reliably predicted by the presence of any of the genes of the\n                    <i>cag<\/i>\n                    pathogenicity island"],"prefix":"10.1136","volume":"43","author":[{"given":"P J","family":"Jenks","sequence":"first","affiliation":[{"name":"aUnit\u00e9 de Pathog\u00e9nie Bact\u00e9rienne des Muqueuses, Pasteur Institute, Paris, France, \n\nbLaboratory of Bacteriology, Pellegrin Hospital, Bordeaux, France"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"F","family":"M\u00e9graud","sequence":"additional","affiliation":[{"name":"aUnit\u00e9 de Pathog\u00e9nie Bact\u00e9rienne des Muqueuses, Pasteur Institute, Paris, France, \n\nbLaboratory of Bacteriology, Pellegrin Hospital, Bordeaux, France"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"A","family":"Labigne","sequence":"additional","affiliation":[{"name":"aUnit\u00e9 de Pathog\u00e9nie Bact\u00e9rienne des Muqueuses, Pasteur Institute, Paris, France, \n\nbLaboratory of Bacteriology, Pellegrin Hospital, Bordeaux, France"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"239","published-online":{"date-parts":[[1998,12,1]]},"reference":[{"key":"2025120520201335000_43.6.752.1","first-page":"1273","article-title":"Unidentified curved bacilli on gastric epithelium in chronic active gastritis.","volume":"i","author":"Warren","year":"1983","journal-title":"Lancet"},{"key":"2025120520201335000_43.6.752.2","doi-asserted-by":"publisher","DOI":"10.1016\/0966-842X(93)90047-U"},{"key":"2025120520201335000_43.6.752.3","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199110173251603"},{"key":"2025120520201335000_43.6.752.4","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199405053301803"},{"key":"2025120520201335000_43.6.752.5","unstructured":"IARC Working Group on the evaluation of carcinogenic risks to humans (1994) Helicobacter pylori. 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