A clinical pathway for gastrectomy patients proved useful to optimize their postoperative care, including medication management and diet education. It is suggested that the implementation of a standardized clinical pathway for gastrectomy patients reduced the length of the hospital stay and the medical costs.
The EGF stimulation system for growth regulation is implicated in normal and neoplastic cell proliferation. The role of EGF, the EGF receptor, and c‐erbB‐2 in human gastric cancer is reviewed on the basis of several reports, which have been mainly oriented toward their clinical significance. EGF has been shown immunohistochemically to be present in 26% of gastric cancers (n = 395). The presence of EGF in gastric cancer is correlated with the degree of gastric wall invasion and lymph node metastasis. The 5‐year survival of patients with EGF‐positive tumors is worse than that of patients with EGF‐negative tumors. The presence of EGF in human gastric cancer may therefore represent a higher malignant potential. Fifteen percent of gastric cancers (n = 352) were also shown to be positive for both EGF and the EGF receptor immunohistochemically, and the simultaneous occurrence of EGF and the EGF receptor suggests that these tumors grow in an autocrine fashion. Tumors exhibiting EGF and the EGF receptor simultaneously show a greater degree of local invasion and lymph node metastasis. Increased expression of EGF receptor protein in gastric cancer appears to be related to biologic aggressiveness, although gene amplification has occurred only to a small extent. Twelve percent of gastric cancers (n = 486) were found to be positive for c‐erbB‐2. This type of tumor has a frequent metastasis, and patients with c‐erbB‐2‐positive cancer have a poorer prognosis than those with c‐erbB‐2‐negative tumors. Selective blockade of the EGF receptor and c‐erbB‐2 from their ligands with monoclonal antibodies (MoAbs) inhibits the growth of human gastric cancer xenografts. These MoAbs may therefore be effective antitumor agents against gastric cancer showing overexpression of EGF receptors or c‐erbB‐2. Cancer 1995;75:1418‐25.
We report an extremely rare case of primary squamous cell carcinoma of the stomach. A 69-year-old man was admitted to our hospital with a 2-month history of dysphagia and tarry stools. Endoscopic examination revealed a cauliflower-shaped protruding mass along the lesser curvature of the gastric cardia. Biopsy of the lesion revealed squamous cell carcinoma of the stomach. Computed tomography revealed a thickened stomach wall and a mass protruding into the gastric lumen. Total gastrectomy with splenectomy, distal pancreatectomy, and Roux-en-Y reconstruction was performed, together with a lower thoracic esophagectomy via a left thoracotomy. Histopathological examination of the specimen revealed well-differentiated squamous cell carcinoma of the stomach. Postoperative follow-up was uneventful for the first 18 months. However, multiple liver metastases and para-aortic lymph node metastasis developed subsequently. Despite systemic combination chemotherapy, the patient died because of progression of the recurrent tumors. Here, we review the characteristics of 56 cases of gastric squamous cell carcinoma reported in Japan.
Bile reflux into the gastric remnant was observed by Bilitec 2000. Mucosal erythema and chronic, active inflammatory cell infiltration in the gastric remnant after gastrectomy may be caused by bile reflux or H. pylori infection, respectively.
Protein disulfide isomerase A3 (PDIA3) is a chaperone protein that supports the folding and processing of synthesized proteins. Its expression is associated with the prognosis of laryngeal cancer, hepatocellular carcinoma, diffuse glioma and uterine cervical cancer. In the present study, the expression levels of PDIA3 and its clinicopathological association were examined in 52 cases of gastric cancer (GC). The expression of PDIA3 was examined by immunohistochemistry and scored using a semi-quantitative method. According to the score, GC samples were classified into PDIA3-High and PDIA3-Low GC. PDIA3-High GC samples were predominantly of the intestinal type. Multivariate survival analysis indicated that PDIA3 expression and cancer stage were independent factors. The overall survival of PDIA3-High GC cases was significantly favorable compared with that of PDIA3-Low GC cases, and this was more evident in cases at an advanced stage. In GC cell cultures, the PDIA3 and major histocompatibility complex (MHC) class I proteins were expressed in three out of the four assessed cell lines according to western blot analysis. Notably, the expression of MHC class I was increased by the stimulation of interferon γ. Co-immunoprecipitation assays suggested the formation of a PDIA3 and MHC class I complex. The findings suggested that PDIA3 may be involved in the immune response of carcinoma cells. The improved prognosis in PDIA3-High GC may be accounted for, in part, by sufficient antigen processing and expression of MHC class I, which can be mediated by PDIA3. It was suggested that PDIA3 serves an important role in the pathobiology of GC, and that PDIA3 is a useful marker for the prediction of prognosis.
The concentrations of cell mediators in the peritoneal and wound fluids of patients who underwent abdominal surgery or mastectomy were determined sequentially and compared with the concomitant changes in blood components. The level of interleukin-6 (IL-6) in the peritoneal and wound fluids was significantly higher than the plasma level after gastrectomy (P < 0.001), cholecystectomy (P < 0.05), and mastectomy (P < 0.05), although the level of plasma IL-6 was also higher postoperatively than before surgery (P < 0.001, P < 0.05). Significantly higher levels of tumor necrosis factor-alpha were detected in the peritoneal and wound fluids (P < 0.01, P < 0.05, respectively) after surgery despite its absence in plasma. A platelet-specific protein and a protein specific for fibroblasts were also measured. Thus, mediators derived from various cells were shown to be present in human peritoneal and wound fluids, indicating that the local production of these mediators plays an important role in the process of tissue repair.
early gastric cancer is metachronous multiple cancer, and H. pylori infection may be a causative factor [3]. Much human and animal evidence has shown a close association between H. pylori infection and gastric cancer [4-6]. Although cancer development is a multifactorial process [7], H. pylori infection increases the risk of gastric cancer. "The Maastricht Consensus Report" strongly recommends H. pylori eradication therapy following early resection for gastric cancer [8]. There are some data showing that H. pylori eradication is associated with a decrease in the recurrence rate in patients with early gastric cancer that is resected endoscopically [9,10]. However, few reports have been published on H. pylori eradication therapy in the remnant stomach [11,12]. In this study, we investigated the following factors in the remnant stomach after distal gastrectomy: (1) the eradication rate of H. pylori in comparison with that in the unoperated stomach, (2) changes in chronic gastritis scores, according to the updated Sydney system [13], after H. pylori eradication therapy, in comparison with scores in the unoperated stomach, and (3) changes in gross endoscopic findings after H. pylori eradication. Patients and methods Patients The remnant stomachs in 137 patients after distal gastrectomy were H. pylori-positive, and 64 were H. pylorinegative; 40 of the H. pylori-positive patients were randomly selected for H. pylori eradication therapy (Table 1). All 40 patients were tested for H. pylori 4-6 weeks after the start of the eradication therapy; 14 of them were followed endoscopically for more than 1 year (average, 21 months) and histological examinations were performed. Among the untreated patients, 22 (15 H. pylori-positive and 7 H. pylori-negative) were endoscopically followed for more than 1 year (average, 32
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