No abstract

The study was conducted to determine expression patterns of microRNA (miRNA), a non-coding RNA that controls gene expression mainly through translational repression, in gastric mucosa infected with Helicobacter pylori. Using endoscopic biopsy specimens, miRNA expression patterns in H. pylori-infected gastric mucosa were determined by microarray. The differentially expressed miRNAs were quantitated by real-time reverse-transcriptase polymerase chain reaction (RT-PCR). An in vitro infection model was assessed to monitor the regulation of miRNAs in gastric epithelium in response to H. pylori. The comprehensive method unraveled the expression profiles; among 470 human miRNAs loaded, 55 were differentially expressed between H. pylori-positive and -negative subjects. The expression levels were significantly decreased in 30 miRNAs, whereas hsa-miRNA-223 was the only miRNA to be overexpressed on quantitative RT-PCR. Eight miRNAs enabled discrimination of H. pylori status with acceptable accuracy. Gastritis scores of activity and chronic inflammation according to the updated Sydney system correlated significantly with the expression levels of diverse miRNAs. Cure of the infection with an anti-H. pylori regimen restored decreased expression in 14 of the 30 miRNAs. Expression levels of some miRNAs, including let-7 family members, were significantly altered following infection with a virulent H. pylori strain carrying intact cag pathogenicity island including cagA but not isogenic mutants. These results provide insights into miRNA involvement in the pathogenesis of H. pylori-associated gastritis. cagA may be involved in cellular regulation of certain miRNAs in the gastric epithelium.

It is known that the signal transducer and activator of transcription 3 (STAT3) is a key signaling molecule implicated in the regulation of growth and malignant transformation. Constitutive activation of STAT3 has been observed in a number of tumour-derived cell lines, as well as in a wide variety of human malignancies. The present study was conducted to examine p-STAT3 (activated form of STAT3) expression and its association with clinicopathological factors and prognosis in human colorectal adenocarcinomas. Expression of p-STAT3 was immunohistochemically examined in 108 cases of colorectal adenocarcinoma tissue obtained at surgery. and was found in 57.4% of tumours (62 of 108). p-STAT3 immunoreactivity significantly correlated with the depth grading of tumour invasion (p<0.001), lymphatic invasion(p<0.05), Dukes' classification (p<0.05), stage (p<0.001) and prognosis after operation (p<0.001). Expression of p-STAT3 was a marker of poor prognosis in overall survival (p<0.01). Expression of p-STAT3 was detected by Western blot analysis in three colon carcinoma tissue samples obtained at surgery.To our knowledge, this is the first study on the poor prognosis of p-STAT3 in human colorectal adenocarcinomas. These findings suggest that expression of p-STAT3 is an important factor related to tumour invasion and poor prognosis of human colorectal adenocarcinoma.

BackgroundEndoscopic submucosal dissection (ESD) permits removal of esophageal epithelial neoplasms en bloc, but is associated with esophageal stenosis, particularly when ESD involves the entire circumference of the esophageal lumen. We examined the effectiveness of systemic steroid administration for control of postprocedural esophageal stricture after complete circular ESD.MethodsSeven patients who underwent wholly circumferential ESD for superficially extended esophageal squamous cell carcinoma were enrolled in this study. In 3 patients, prophylactic endoscopic balloon dilatation (EBD) was started on the third post-ESD day and was performed twice a week for 8 weeks. In 4 patients, oral prednisolone was started with 30 mg daily on the third post-ESD day, tapered gradually (daily 30, 30, 25, 25, 20, 15, 10, 5 mg for 7 days each), and then discontinued at 8 weeks. EBD was used as needed whenever patients complained of dysphagia.ResultsEn bloc ESD with tumor-free margins was safely achieved in all cases. Patients in the prophylactic EBD group required a mean of 32.7 EBD sessions; the postprocedural stricture was dilated up to 18 mm in diameter in these patients. On the other hand, systemic steroid administration substantially reduced or eliminated the need for EBD. Corticosteroid therapy was not associated with any adverse events. Post-ESD esophageal stricture after complete circular ESD was persistent, requiring multiple EBD sessions.ConclusionsUse of oral prednisolone administration may be an effective treatment strategy for reducing post-ESD esophageal stricture after complete circular ESD.

Background: The signal transducer and activator of transcription 3 (STAT3) is a key signalling molecule implicated in the regulation of growth and malignant transformation. Constitutive activation of STAT3 is seen in several tumour derived cell lines, and in a wide variety of human malignancies. Aims: To examine the relation between p-STAT3 (activated form of STAT3) expression and clinicopathological factors in human colorectal adenocarcinoma and adenoma. Methods: Immunohistochemical analyses were carried out on tissues from 44 colorectal adenomas and 95 colorectal adenocarcinomas, comprising 18 intramucosal carcinomas and 77 invasive carcinomas. Results: Seventy seven of these 139 samples (55.4%) showed immunoreactivity for p-STAT3. Positive staining for p-STAT3 was seen in 69 of the 95 carcinomas. Only eight of the 44 adenomas showed immunopositivity for p-STAT3, resulting in a significant difference between total adenocarcinomas and adenomas (p , 0.001). Among the 95 cases of colorectal adenocarcinoma, p-STAT3 immunoreactivity was significantly correlated with the depth of tumour invasion (p , 0.05), venous invasion (p , 0.05), lymph node metastasis (p , 0.05), and increasing stages of the Dukes' classification (p , 0.01). Expression of p-STAT3 was detected by Western blot analysis in two different cultured human colorectal carcinoma cell lines and six colon carcinoma tissue samples obtained at surgery.