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We aimed to increase understanding of the molecular details of atrophy by performing a global transcriptome analysis of stomach tissue.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Methods<\/jats:title>\n            <jats:p>Biopsies from patients with different stages of <jats:italic>H. pylori<\/jats:italic> infection were taken from both the antrum and corpus mucosa and analyzed on microarrays. The stages included patients without current <jats:italic>H. pylori<\/jats:italic> infection, <jats:italic>H. pylori<\/jats:italic>-infected without corpus atrophy and patients with current or past <jats:italic>H. pylori<\/jats:italic>-infection with corpus-predominant atrophic gastritis.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Results<\/jats:title>\n            <jats:p>Using clustering and integrated analysis, we found firm evidence for antralization of the corpus mucosa of atrophy patients. This antralization harbored gain of gastrin expression, as well as loss of expression of corpus-related genes, such as genes associated with acid production, energy metabolism and blood clotting. The analyses provided detailed molecular evidence for simultaneous intestinal metaplasia (IM) and spasmolytic polypeptide expressing metaplasia (SPEM) in atrophic corpus tissue. Finally, acidic mammalian chitinase, a chitin-degrading enzyme produced by chief cells, was shown to be strongly down-regulated in corpus atrophy.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Conclusions<\/jats:title>\n            <jats:p>Transcriptome analysis revealed several gene groups which are related to development of corpus atrophy, some of which were increased also in <jats:italic>H. pylori<\/jats:italic>-infected non-atrophic patients. Furthermore, loss of acidic chitinase expression is a promising marker for corpus atrophy.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1186\/1755-8794-6-41","type":"journal-article","created":{"date-parts":[[2013,10,12]],"date-time":"2013-10-12T03:08:32Z","timestamp":1381547312000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":62,"title":["Transcriptome signatures in Helicobacter pylori-infected mucosa identifies acidic mammalian chitinase loss as a corpus atrophy marker"],"prefix":"10.1186","volume":"6","author":[{"given":"Intawat","family":"Nookaew","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kaisa","family":"Thorell","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kuntal","family":"Worah","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shugui","family":"Wang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Martin Lloyd","family":"Hibberd","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Henrik","family":"Sj\u00f6vall","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sven","family":"Pettersson","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jens","family":"Nielsen","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Samuel B","family":"Lundin","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2013,10,11]]},"reference":[{"issue":"4","key":"418_CR1","doi-asserted-by":"publisher","first-page":"713","DOI":"10.1128\/CMR.00011-10","volume":"23","author":"LE Wroblewski","year":"2010","unstructured":"Wroblewski LE, Peek RM, Wilson KT: Helicobacter pylori and gastric cancer: factors that modulate disease risk. 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