18F-fluorodeoxyglucose positron emission tomography/computed tomography-based radiomic features for prediction of epidermal growth factor receptor mutation status and prognosis in patients with lung adenocarcinoma.

BACKGROUND: To investigate whether radiomic features from (18F)-fluorodeoxyglucose positron emission tomography/computed tomography [(18F)-FDG PET/CT] can predict epidermal growth factor receptor (EGFR) mutation status and prognosis in patients with lung adenocarcinoma. METHODS: One hundred and seventy-four consecutive patients with lung adenocarcinoma underwent (18F)-FDG PET/CT and EGFR gene testing were retrospectively analyzed. Radiomic features combined with clinicopathological factors to construct a random forest (RF) model to identify EGFR mutation status. The mutant/wild-type model was trained on a training group (n=139) and validated in an independent validation group (n=35). The second RF classifier predicting the 19/21 mutation site was also built and evaluated in an EGFR mutation subset (training group, n=80; validation group, n=25). Radiomic score and 5 clinicopathological factors were integrated into a multivariate Cox proportional hazard (CPH) model for predicting overall survival (OS). AUC (the area under the receiver characteristic curve) and C-index were calculated to evaluate the model's performance. RESULTS: Of 174 patients, 109 (62.6%) harbored EGFR mutations, 21L858R was the most common mutation type [55.9% (61/109)]. The mutant/wild-type model was identified in the training (AUC, 0.77) and validation (AUC, 0.71) groups. The 19/21 mutation site model had an AUC of 0.82 and 0.73 in the training and validation groups, respectively. The C-index of the CPH model was 0.757. The survival time between targeted therapy and chemotherapy for patients with EGFR mutations was significantly different (P=0.03). CONCLUSIONS: Radiomic features based on (18F)-FDG PET/CT combined with clinicopathological factors could reflect genetic differences and predict EGFR mutation type and prognosis.

MicroRNA-146a enhances Helicobacter pylori induced cell apoptosis in human gastric cancer epithelial cells.

Helicobacter pylori (H. pylori) infection induces apoptosis in gastric epithelial cells, and this occurrence may link to gastric carcinogenesis. However, the regulatory mechanism of H. pylori-induced apoptosis is not clear. MicroRNA-146a has been implicated as a key regulator of the immune system. This report describes our discovery of molecular mechanisms of microRNA-146a regulation of apoptosis in human gastric cancer cells. We found that overexpression of microRNA-146a by transfecting microRNA-146a mimics could significantly enhance apoptosis, and this up-regulation was triggered by COX-2 inhibition. Furthermore, we found that microRNA-146a density was positively correlated with apoptosis rates in H. pylori-positive gastric cancer tissues and intratumoral microRNA-146a density was negatively correlated with lymph node metastasis among H. pylori-positive gastric cancer patients. Understanding the important roles of microRNA-146a in regulating cell apoptosis in H. pylori infected human gastric cancer cells will contribute to the development of microRNA targeted therapy in the future.

[Plasma levels of vWF and NO in patients with metabolic syndrome and their relationship with metabolic disorders].

OBJECTIVE: To measure the plasma levels of von Willebrand factor (vWF) and nitric oxide (NO) in patients with metabolic disorders and to study their relationships with the disease. METHODS: The plasma levels of vWF and NO were determined in patients with metabolic syndrome (MS group, n=36), patients with 1 - 2 metabolic disorders (MD group, n=43) and normal subjects (control group, n=30). RESULT: The plasma vWF level was higher in MS group than that in MD group (P <0.05) and in control group (P <0.001); the vWF level in MD group was higher than that in control group (P <0.05). The NO level was lower in MS group and in MD group than that in control group (both P<0.05), while the difference between MS and MD groups was not statistically significant (P >0.05). Multiple stepwise regression showed that vWF level was correlated with systolic BP (SBP), diastolic BP(DBP) and pulse BP; that NO level was correlated with BMI, SBP and TG. CONCLUSION: Multiple metabolic disorders of metabolic syndrome may injure endothelial cells, and the degree of endothelial cell injury seems to be correlated with the BMI, SBP, DBP, pulse BP and TG.