Hiroaki Takeo1, Susumu Matsukuma. 1. Japan Self Defense Forces Central Hospital, Tokyo, Japan. hiroakitk6@hotmail.com
Abstract
BACKGROUND AND AIM: Gastric tube cancer (GTC), defined as carcinoma arising in the reconstructed gastric tube after esophagectomy, has been increasingly reported, but its pathogenesis remains unclear. Therefore, the aim of this study was to examine clinically and pathologically 10 GTCs in six patients. METHODS: In addition to examination of the clinicopathological features of GTCs, the adjacent gastric tube mucosa was also evaluated immunohistochemically using gastric foveolar markers (MUC5AC and human gastric mucin), pyloric gland markers (MUC6 and M-GGMC-1), and intestinal markers (MUC2 and CD10). RESULTS: All patients were men and three patients had multiple GTCs. All GTCs were located on the middle to lower portion of the gastric tube. Nine GTCs had tubular and/or papillary adenocarcinoma components, and another was signet-ring cell carcinoma. Intestinal metaplasia was found in non-neoplastic mucosa adjacent to nine GTCs. Metaplastic goblet cells adjacent to five GTCs expressed both gastric and intestinal markers, which were similar to the corresponding GTC cells, indicating a close association between the GTCs and metaplastic goblet cells. The other three GTCs expressed only intestinal markers, which may support the suggestion that the intestinal phenotype is expressed later in cancerous development. CONCLUSION: Pathogenesis of GTCs could be identical to that of ordinary gastric cancer. Cancerous multiplicity associated with esophageal cancer may also play a role in the development of GTCs.
BACKGROUND AND AIM: Gastric tube cancer (GTC), defined as carcinoma arising in the reconstructed gastric tube after esophagectomy, has been increasingly reported, but its pathogenesis remains unclear. Therefore, the aim of this study was to examine clinically and pathologically 10 GTCs in six patients. METHODS: In addition to examination of the clinicopathological features of GTCs, the adjacent gastric tube mucosa was also evaluated immunohistochemically using gastric foveolar markers (MUC5AC and humangastric mucin), pyloric gland markers (MUC6 and M-GGMC-1), and intestinal markers (MUC2 and CD10). RESULTS: All patients were men and three patients had multiple GTCs. All GTCs were located on the middle to lower portion of the gastric tube. Nine GTCs had tubular and/or papillary adenocarcinoma components, and another was signet-ring cell carcinoma. Intestinal metaplasia was found in non-neoplastic mucosa adjacent to nine GTCs. Metaplastic goblet cells adjacent to five GTCs expressed both gastric and intestinal markers, which were similar to the corresponding GTC cells, indicating a close association between the GTCs and metaplastic goblet cells. The other three GTCs expressed only intestinal markers, which may support the suggestion that the intestinal phenotype is expressed later in cancerous development. CONCLUSION: Pathogenesis of GTCs could be identical to that of ordinary gastric cancer. Cancerous multiplicity associated with esophageal cancer may also play a role in the development of GTCs.