Research Papers:
Identification of AQP3 and CD24 as biomarkers for carcinogenesis of gastric intestinal metaplasia
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Abstract
Haijian Zhao1,2,*, Jianfei Wen1,*, Xuqiang Dong1,*, Ruji He1,*, Cheng Gao1, Weiming Zhang3, Zhihong Zhang3 and Lizong Shen1
1Division of Gastrointestinal Surgery, Department of General Surgery, First Affiliated Hospital, Nanjing Medical University, Nanjing 210029, Jiangsu, China
2Division of Gastrointestinal Surgery, Department of General Surgery, Affiliated Huai’an Hospital, Xuzhou Medical University, Huai’an 223002, Jiangsu, China
3Department of Pathology, First Affiliated Hospital, Nanjing Medical University, Nanjing 210029, Jiangsu, China
*These authors have contributed equally to this work
Correspondance to:
Lizong Shen, email: [email protected]
Keywords: gastric intestinal metaplasia, aquaporin 3, CD24, gastric cancer, pathology
Received: December 16, 2016 Accepted: June 02, 2017 Published: June 28, 2017
ABSTRACT
Gastric intestinal metaplasia (GIM) is a precancerous gastric carcinoma (GC) lesion with pivotal roles in carcinogenesis. CD24, LGR5 and Ki67 are expressed in GIM; we previously demonstrated that aquaporin 3 (AQP3) is expressed in goblet cells and is positively correlated with GIM severity. However, the relationships of AQP3 with GIM classification and with other proteins, and their roles in the transition from GIM to gastric carcinoma (GC) remain unknown. Sixteen patients with intestinal-type GC were enrolled in this study. GIM was determined according to the updated Sydney system; GIM classification was determined via HID-AB staining, and AQP3, CD24, LGR5 and Ki67 expression were determined by immunohistochemistry. Type III GIM was more prevalent around the GC and displayed a positive association with GIM severity. CD24 was found in GIM, but LGR5 and Ki67 were found in tissues regardless of GIM. AQP3 expression showed significant correlation to type III GIM. CD24 expression was correlated with the marked GIM and incomplete GIM, while LGR5 expression decreased with GIM aggravation and did not have relationship with classification of GIM. However, Ki67 presented no association with GIM grade or classification. These observations identify AQP3 and CD24 as biomarkers for carcinogenesis of GIM, and may provide a precise strategy for screening at-risk candidates with GIM.
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