Potential role of aquaporin 3 in gastric intestinal metaplasia
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Haijian Zhao1,2, Xiaojun Yang3, Yangchun Zhou1,4, Weiming Zhang5, Yao Wang1, Jianfei Wen1, Zhihong Zhang5, Lizong Shen1
1Division of Gastrointestinal Surgery, Department of General Surgery, First Affiliated Hospital, Nanjing Medical University, Nanjing 210029, Jiangsu, China
2Department of Gastrointestinal Surgery, Huai’an Hospital Affiliated to Xuzhou Medical College, Second People’s Hospital of Huai’an City, Huai’an 223002, Jiangsu, China
3Department of General Surgery, Second Affiliated Hospital, Nanjing Medical University, Nanjing 210011, Jiangsu, China
4Department of General Surgery, Affiliated Mingde Hospital, Nanjing Medical University, Nanjing 211166, Jiangsu, China
5Department of Pathology, First Affiliated Hospital, Nanjing Medical University, Nanjing 210029, Jiangsu, China
Lizong Shen, e-mail: email@example.com
Keywords: gastric intestinal metaplasia, aquaporin 3, gastric cancer, pathology
Received: June 25, 2015 Accepted: August 30, 2015 Published: October 16, 2015
Gastric intestinal metaplasia (GIM) is a pre-cancerous condition and a pivotal step in the formation of gastric cancer (GC). Aquaporin 3 (AQP3) has been found to be expressed in goblet cells rather than mucus-secreting glands. To investigate the characteristics of GIM in non-cancerous tissues adjacent to GC, as well as the expression and role of AQP3 in GIM tissues, 16 patients diagnosed with gastric adenocarcinoma of intestinal type located in the lesser curve of the antrum were consecutively enrolled in this study. A new pathological technology called “gastric mucosal sausage roll” was introduced. GIM was determined according to the updated Sydney system, and AQP3 expression in goblet cells was determined by immunohistochemistry. GIM was found in all stomach specimens, and its incidence increased with progression to GC (P < 0.001). GIM prevalence displayed remarkable association with the distance to GC in the anterior gastric wall tissues (P = 0.016) and tissues toward the cardia (P = 0.014), such that GIM was more common in the areas closer to GC (P < 0.001). AQP3 was found to be expressed in 67.71% of parts with GIM, and AQP3 immunoreactivity was identified more frequently in severe GIM areas (P < 0.001). In short, the incidence and severity of GIM correlated with the distance from GC, and AQP3 was differentially expressed in goblet cells, with most AQP3-positive goblet cells presenting in severe GIM. Together, this study suggests that AQP3 may play an important role in gastric carcinogenesis from GIM.
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