ABSTRACT
A 60-year-old woman was admitted for the treatment of a gastric neuroendocrine tumor (NET) associated with type A chronic atrophic gastritis. The lesion measured 10 mm in diameter, and a computed tomography scan did not reveal any metastatic lesions. Endoscopic submucosal dissection (ESD) was subsequently performed. A histological examination revealed three gastric NETs, two of which exhibited vessel invasion. Endocrine cell micronests associated with a high risk of recurrence were also observed. Therefore, the patient underwent total gastrectomy with lymph node dissection. Because vessel invasion can occur in patients with small gastric NET G1, the use of ESD should be considered to carefully estimate the presence of invasion.
Subject(s)
Lymphatic Metastasis/diagnosis , Neovascularization, Pathologic/diagnosis , Neuroendocrine Tumors/diagnosis , Stomach Neoplasms/diagnosis , Endoscopy, Digestive System , Female , Gastrectomy , Gastritis, Atrophic/complications , Humans , Incidence , Lymph Node Excision , Middle Aged , Neoplasm Recurrence, Local/epidemiology , Neoplasm Recurrence, Local/prevention & control , Neovascularization, Pathologic/etiology , Neovascularization, Pathologic/surgery , Neuroendocrine Tumors/etiology , Neuroendocrine Tumors/surgery , Stomach Neoplasms/etiology , Stomach Neoplasms/surgery , Treatment OutcomeABSTRACT
Recent advances in endoscopic submucosal dissection (ESD) techniques contribute to endoscopic treatment of early gastric cancer (EGC). Recognition of chronic atrophic gastritis as the background is important for high-quality detection and diagnosis of EGC. But, relationships between EGC and atrophy of the background gastric mucosa caused by Helicobacter pylori are not well understood. The present study demonstrated histopathological phenotypes of EGC, as well as chronic atrophic gastritis as background mucosa of EGC. We evaluated mucosal heights, number of glands, and degree of intestinal metaplasia (IM) of the background gastric mucosa, using 81 cases of EGC resected by ESD. Gastric phenotype cancer cases showed IM of the background gastric mucosa less frequently, compared with intestinal phenotype cancer cases (score of IM, 1.15 vs. 1.65, P = 0.012). The average mucosal heights around EGC were lower in moderately to poorly differentiated adenocarcinoma cases than well differentiated adenocarcinoma cases (442.6 µm vs. 500.2 µm, P = 0.011). The mucosal atrophy indicated by average heights of background mucosa was low in the gastric phenotype cancer cases, compared with the intestinal phenotype cancercases (452.8 µm vs. 505.6 µm, P = 0.018). In the fundic gland area, the mucosal heights were low in the gastric phenotype cancer cases, compared with the intestinal phenotype cancer cases (413.2 µm vs. 495.5 µm, P = 0.015). Our results using EGC specimens indicated that gastric phenotype cancer and moderately to poorly differentiated adenocarcinoma had atrophic background mucosa with lower mucosal heights and less IM. The atrophic gastric mucosa with less IM is thought to play an important role in gastric carcinogenesis, especially tumoriogenesis of gastricphenotype cancer.
Subject(s)
Gastric Mucosa/pathology , Gastritis, Atrophic/pathology , Intestinal Neoplasms/pathology , Stomach Neoplasms/pathology , Adenocarcinoma/pathology , Aged , Atrophy/pathology , Cell Transformation, Neoplastic/pathology , Female , Gastritis, Atrophic/complications , Helicobacter Infections/microbiology , Helicobacter Infections/pathology , Helicobacter pylori/physiology , Humans , Intestines/pathology , Japan , Male , Metaplasia/pathology , Precancerous Conditions/pathology , Stomach/pathologyABSTRACT
BACKGROUND AND OBJECTIVES: Pancreatic ductal adenocarcinoma (PDAC) is one of the most extremely aggressive cancers with a poor prognosis after curative resection. L1 cell adhesion molecule (L1CAM) is a 200-220 kDa type I transmembrane glycoprotein of the immunoglobulin superfamily, which has been shown to affect the prognosis of several cancers. No clinicopathological significance of L1CAM expression has been examined at the invasive front of PDAC. In this study, we examined the relationship between L1CAM expression and clinicopathological features in PDAC by immunohistochemistry. METHODS: One hundred seven surgically resected specimens of PDAC were immunohistochemically examined using a monoclonal antibody against L1CAM. RESULTS: Positive expression of L1CAM was found in 23 of 107 cases with PDAC. In most cases (21/23), L1CAM expression was localized at the invasive front of the tumor tissue. Positive expression of L1CAM was significantly correlated with the histological grade, lymph node involvement, and distant metastasis. In univariate analysis, a positive expression of L1CAM was associated with short overall survival (P = 0.0002), and this was significant in multivariate analysis (P = 0.009). CONCLUSIONS: L1CAM could play an important role in the invasive process in vivo, and is thought to be a good indicator of prognosis in PDAC.