Abstract
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.
Highlights
The incidence of gastric cancer (GC) has decreased over the past decades, it remains one of the most common cancers and the third leading cause of cancer-related mortality worldwide [1]
Previous studies that defined the relationship between Gastric intestinal metaplasia (GIM) and GC were mostly based on the long-term follow-up of a cohort of patients by histological examination of gastric biopsies obtained under upper endoscopy, yet the pathogenesis of GIM in gastric carcinogenesis is still unclear [14,15,16,17]
Sixty-four gastric mucosal sausage rolls were obtained from 16 GC patients, and 192 parts were evaluated for severity of GIM
Summary
The incidence of gastric cancer (GC) has decreased over the past decades, it remains one of the most common cancers and the third leading cause of cancer-related mortality worldwide [1]. Gastric intestinal metaplasia (GIM), derived mainly from gastric antrum [8], is recognized as a pre-cancerous lesion of GC and a pivotal point in gastric carcinogenesis [9, 10], with GIM patients eventually progressing into intestinal type gastric carcinoma [7, 11,12,13]. Previous studies that defined the relationship between GIM and GC were mostly based on the long-term follow-up of a cohort of patients by histological examination of gastric biopsies obtained under upper endoscopy, yet the pathogenesis of GIM in gastric carcinogenesis is still unclear [14,15,16,17]
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