Plasma-Methylated SEPT9 for the Noninvasive Diagnosis of Gastric Cancer.

BACKGROUND: Gastric cancer (GC) is one of the most prevalent cancers globally. This study was designed to evaluate the potential performance of plasma SEPT9 methylation (mSEPT9) as a noninvasive biomarker for the diagnosis of GC. METHODS: A total of 182 participants, i.e., 60 patients with GC, 39 with chronic superficial gastritis (CSG), 27 with chronic atrophic gastritis (CAG), 30 with gastric ulcer (GU), and 26 with gastric polys (GP), were recruited. The mSEPT9 level was measured using real-time polymerase chain reaction. RESULTS: As a diagnostic target, mSEPT9 (1/3 algorithm) had a sensitivity of 48.33 (95% confidence interval (CI): 35.40-61.48%) and a specificity of 86.89% (95% CI: 79.28-92.09%), and mSEPT9 (2/3 algorithm) had a sensitivity of 33.33 (95% CI: 22.02-46.79%) and a specificity of 98.36% (95% CI: 93.61-99.72%). The area under the receiver operating characteristic curve (ROC) curve of mSEPT9 was 0.698 (95% CI: 0.609-0.787) for the differentiation of GC from benign gastric diseases. The effectiveness of mSEPT9 (1/3 algorithm) was superior to that of CEA, CA19-9, and CA72-4. mSEPT9 was positively correlated with T, N, M, and the clinical stage of GC. CONCLUSIONS: Plasma mSEPT9 might serve as a useful and noninvasive biomarker for the diagnosis of GC.

Plasma Methylated RNF180 for Noninvasive Diagnosis of Gastric Cancer.

Background: RNF180 is a tumor suppressor gene involved in cell development, proliferation, and apoptosis. Methylation of RNF180 (mRNF180) leads to low expression of RNF180, which is closely related to the occurrence and development of gastric cancer (GC). This study was designed to evaluate the potential performance of plasma mRNF180 as noninvasive biomarker for the diagnosis of GC. Methods: A total of 156 participants, including 60 patients with GC, 39 with chronic superficial gastritis (CSG), 27 with chronic atrophic gastritis (CAG), and 30 with gastric ulcer (GU) were recruited for this study. Plasma mRNF180 level was measured using real-time polymerase chain reaction. Results: As a diagnostic target, mRNF180 had a sensitivity of 71.67% (95% CI: 58.36%-82.18%) and specificity of 59.38% (95% CI: 48.85%-69.14%). The area under the ROC curve value of mRNF180 was 0.731 (95% CI: 0.648%-0.813%) for differentiation of GC from benign gastric diseases (BGD). The effectiveness of mRNF180 was superior to that of CEA, CA199, and CA724. mRNF180 was positively correlated with age, tumor size, T stage, N stage, M stage, and clinical stage of patients with GC. Conclusions: Plasma mRNF180 might serve as a useful and noninvasive biomarker for the diagnosis of GC and can be used to evaluate its prognosis.

The relationship between gastric microbiota and gastric disease.

Traditionally, the stomach was believed to be a sterile organ unsuitable for microbiota growth. However, the discovery of H. pylori subverted this conception. With the development of molecular techniques, an abundance of microbiota of great diversity was found in the stomach. In addition, various lines of evidence suggest that the gastric microbiota plays a critical role in the development and progression of the gastric disease.The gastrointestinal microbiome plays an important role in various physiologic and pathologic processes.

Ulcerative colitis with mucosal lesions in duodenum: Two case reports.

RATIONALE: Ulcerative colitis (UC) is a chronic, nonspecific, inflammatory disease of the colon. Colorectal is the main target organ of UC, while other digestive tract involvement is rare. This report describes 2 rare cases of duodenal mucosa lesions in patients with UC after total colectomy. PATIENT CONCERNS: In case 1, a patient of 45-year-old with intermittent diarrhea and bloody mucosanguineous feces who was diagnosed as UC, revealed diffuse erosive ulcers in the descending duodenum through gastroscopy after total colectomy. In case 2, a 55-year-old Chinese female with UC, aggravated to colon cancer and received total colectomy. Eighteen months after surgery, the patient was admitted to hospital following upper abdominal pain and acid regurgitation. A gastroscopy found inflammation in the descending part of the duodenum. DIAGNOSIS: UC, duodenal mucosa lesions INTERVENTIONS:: In case 1, the patient was treated with oral mesalazine (1 g/tid) and hydrocortisone (0.3 g/d) but symptoms did not improve, and the treatment was changed to oral methylprednisolone (0.6 g/d) and a hydrocortisone enema (0.1 g/late). Finally, the patient underwent a total colectomy and ileostomy. In case 2, the patient was treated with sulfasalazine, mesalazine, and intermittent hormone enemas. A total colectomy and ileostomy were performed with the patient after diagnosed as colon cancer. After surgery, the patient received N1-(2 tetrahydrofuryl)-5-fluorouracil (FT-207), 8 g, 300 mg, and 100 mg oxaliplatin chemotherapy, and biologic therapy. OUTCOMES: In case 1, the patient presented with duodenal necrosis and died of septic shock. In case 2, the patient recovered well without recurrence by taking proton pump inhibitor. LESSONS: The occurrence of UC related ulcerative gastroduodenal mucosal lesions may be associated with progressing UC or total colitis that does not respond to hormone therapy, leading to requirement of total colectomy.

[Expression of human beta-defensin 2 and tumor necrosis factor-A in colonic mucosae of ulcerative colitis and diarrhea-predominant irritable bowel syndrome].

OBJECTIVE: To detect the expression of human beta-defensin 2 (HBD-2) and tumor necrosis factor-alpha (TNF-alpha) in the colonic mucosae of ulcerative colitis (UC) patients and diarrhea-predominant irritable bowel syndrome (IBS-D) patients and to evaluate the roles of HBD-2 and TNF-alpha in the pathogenesis and the relationship between them. METHODS: Immunohistochemistry was conducted on the biopsy samples of colonic mucosa from 30 UC patients, 20 IBS-D patients, and 10 normal persons to measure the expression of HBD-2 and TNF-alpha. RESULTS: The expression levels of HBD-2 and TNF-alpha in the colonic mucosa of UC were both significantly higher than those in the colonic mucosa of IBS-D (z = -4.856, z = -3. 987, all P < 0.01) and in the normal colonic mucosa (z = -3.611, z = -3. 248, all P < 0.01). But no significant differences were found between the colonic mucosa of IBS-D and the normal colonic mucosa in the intensity of the expressions of HBD-2 and TNF-alpha (z = -0.373, z = -0.032, all P > 0.05). There were no significant differences in the intensity of the expressions of HBD-2 and TNF-alpha in colonic mucosa of among the mild, moderate, and severe UC (chi2 = 1.190, P > 0.05, chi2 = 1.672, P > 0. 05). CONCLUSION: The expressions of HBD-2 and TNF-at are significantly increased in UC, but are not correlated with IBS-D and the severity of clinical symptoms of UC patients.