Expression of CDX2 in gastric cardia adenocarcinoma and its correlation with H. pylori and cell proliferation
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Ying Zhang1,*, Hu Wang2,*, Chao Bi1, Yinping Xiao1, Zhaoyong Liu2
1Department of Pathology, Shantou University Medical College, Shantou, Guangdong Province, China
2Department of Orthopaedics, First Affiliated Hospital of Shantou University Medical College, Shantou, Guangdong Province, China
*These authors have contributed equally to this work
Zhaoyong Liu, email: firstname.lastname@example.org
Key words: CDX2, Helicobacter pylori, gastric cardia cancer, cell proliferation
Received: August 30, 2015 Accepted: June 12, 2016 Published: July 1, 2016
Background: Gastric cardia cancer (GCC) is located in the distal stomach, and strongly correlates with atrophic gastritis and Helicobacter pylori (H.pylori) infection. Caudal-related homeobox transcription factor 2 (CDX2) is homeobox gene encoding an intestine-specific transcription factor usually expressed in the intestinal epithelium cells. However, in several recent published papers, CDX2 was found to be aberrantly expressed in gastric, thyroid and ovarian cancer.
Results: Higher expression of CDX2 was found in GCC tissues in comparison with non-malignant cardia mucosa (p<0.05). Moreover, immunohistochemical analysis demonstrated that CDX2 expression correlated with lymphatic metastasis. In addition, we found that CDX2 expression progressively increased with the level of H. pylori infection (p<0.05), and also correlated with cell proliferation, based on Ki67 staining.
Methods: To investigate the relationship between CDX2, cell proliferation and H. pylori infection, we detected CDX2, Ki62 and H.pylori expression in 83 non-malignant gastric cardia mucosacases and 60 GCC specimens in the Chaoshan area, a high-risk region for esophageal and gastric cardia cancer.
Conclusion: These findings provide pathological evidence that H. pylori infectionis a driving force of gastric cardia carcinogenesis by upregulating CDX2 and inducing inflammation. These results provide new pathological evidence that H. pylori infection induces GCC tumorigenesis.
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