The combined presence of<i>H pylori</i>infection and gastro-oesophageal reflux disease leads to an up-regulation of<i>CDX2</i>gene expression in antrum and cardia

Bornschein, Jan; Wex, Thomas; Peitz, Ulrich; Kuester, Doerthe; Roessner, Albert; Malfertheiner, Peter

doi:10.1136/jcp.2008.060061

Cited by 11 publications

(8 citation statements)

References 31 publications

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“…The prevalence of intestinal metaplasia in the stomach, however, is highest when both factors are present: H. pylori and bile reflux [17,18]. This is in line with previously published data showing the highest upregulation of CDX2 in antrum and cardia of patients with both positive H. pylori status and gastro-oesophageal reflux disease [19]. In these cases, the induction of CDX2 as the main driver of intestinal metaplasia seems to be mediated by distinct mechanisms as in the presence of H. pylori infection, the CDX2 expression correlates positively with the degree of the mucosal infiltration with immune cells, whereas the reflux-induced expression of CDX2 is independent of the mucosal inflammation [19].…”

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confidence: 89%

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Bornschein

2015

European Journal of Gastroenterology &Amp; Hepatology

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There are no conflicts of interest. References1 Bornschein J, Dingwerth A, Selgrad M, Venerito M, Stuebs P, Frauenschlaeger K, et al. Adenocarcinomas at different positions at the gastro-oesophageal junction show distinct association with gastritis and gastric preneoplastic conditions. Eur J Gastroenterol Hepatol 2015; 27:492-500. 2 McColl KE, Watabe H, Derakhshan MH. Role of gastric atrophy in mediating negative association between Helicobacter pylori infection and reflux oesophagitis, Barrett's oesophagus and oesophageal adenocarcinoma. Gut 2008; 57:721-723. 3 Anderson LA, Murphy SJ, Johnston BT, Watson RG, Ferguson HR, Bamford KB, et al. Relationship between Helicobacter pylori infection and gastric atrophy and the stages of the oesophageal inflammation, metaplasia, adenocarcinoma sequence: results from the FINBAR case-control study. Gut 2008; 57:734-739. 4 Ye W, Held M, Lagergren J, Engstrand L, Blot WJ, McLaughlin JK, Nyrén O. Helicobacter pylori infection and gastric atrophy: risk of adenocarcinoma and squamous-cell carcinoma of the esophagus and adenocarcinoma of the gastric cardia.

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confidence: 89%

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Bornschein

2015

European Journal of Gastroenterology &Amp; Hepatology

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“…The prevalence of IM in the gastric corpus is usually lower than in the antrum or the cardia which can partially be explained by the different mucosal architecture of these parts of the stomach [47,48]. There might be methodological bias due to the biopsy protocol of the updated Sydney classification.…”

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confidence: 99%

H. pylori Infection Is a Key Risk Factor for Proximal Gastric Cancer

et al. 2010

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“…This is typified in Barrett's esophagus leading to esophageal adenocarcinoma [8], Helicobacter pylori-driven gastric ulcers leading to gastric cancer [9] and chronic long-term ulcerative colitis leading to colon cancer [10]. In breast cancer 1/2, early onset (BRCA1/2) associated breast cancers, tumor-associated CI may provide prognostic value [11].…”

Section: Inflammatory States Promoting Tumor Initiation and Growthmentioning

confidence: 99%

New Insights on COX-2 in Chronic Inflammation Driving Breast Cancer Growth and Metastasis

Hugo

Saunders

Ramsay

et al. 2015

J Mammary Gland Biol Neoplasia

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The medicinal use of aspirin stretches back to ancient times, before it was manufactured in its pure form in the late 19th century. Its accepted mechanistic target, cyclooxygenase (COX), was discovered in the 1970s and since this landmark discovery, the therapeutic application of aspirin and other non-steroidal anti-inflammatory drugs (NSAIDs) has increased dramatically. The most significant benefits of NSAIDs are in conditions involving chronic inflammation (CI). Given the recognized role of CI in cancer development, the use of long-term NSAID treatment in the prevention of cancer is an enticing possibility. COX-2 is a key driver of CI, and here we review COX-2 expression as a predictor of survival in various cancer types, including breast. Obesity and post-partum involution are natural inflammatory states that are associated with increased breast cancer risk. We outline the COX-2 mediated mechanisms contributing to the growth of cancers. We dissect the cellular mechanism of epithelial-mesenchymal transition (EMT) and how COX-2 may induce this to facilitate tumor progression. Finally we examine the potential regulation of COX-2 by c-Myb, and the possible interplay between c-Myb/COX-2 in proliferation, and hypoxia inducible factor-1 alpha (HIF1α)/COX-2 in invasive pathways in breast cancer.

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The combined presence ofH pyloriinfection and gastro-oesophageal reflux disease leads to an up-regulation ofCDX2gene expression in antrum and cardia

Abstract: The combined presence of H pylori infection and GORD leads to an up-regulation of CDX2 gene expression in cardia and antral mucosa, but not in the corpus.

Cited by 11 publications

References 31 publications

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H. pylori Infection Is a Key Risk Factor for Proximal Gastric Cancer

New Insights on COX-2 in Chronic Inflammation Driving Breast Cancer Growth and Metastasis

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