Usefulness of bevacizumab-induced hypertension in patients with metastatic colorectal cancer: an updated meta-analysis.

We tested the hypothesis that bevacizumab-induced hypertension may be a useful predictor for objective response rate, progression-free and overall survival in patients with metastatic colorectal cancer via a comprehensive meta-analysis. Search process, article selection and data extraction were independently performed by two investigators. Statistical analyses were conducted using the STATA/SE software. Fourteen independent studies and 2292 study subjects were synthesized. Overall relative risk of objective response rate for bevacizumab-induced hypertension was 2.03 (95% confidence interval [CI]: 1.18-3.48, p=0.01), with significant heterogeneity and publication bias, whereas unbiased estimate was nonsignificant after considering potentially missing studies. Overall hazard ratio for progression-free survival was 0.58 (95% CI: 0.43-0.77, p<0.001), with significant heterogeneity and publication bias, and unbiased estimate was significant (hazard ratio: 0.52, 95% CI: 0.41-0.66, p<0.001). Overall hazard ratio for overall survival was 0.51 (95% CI: 0.39-0.65, p<0.001), and this estimate was not likely confounded by heterogeneity or publication bias. Subgroup and meta-regression analyses suggested that hypertension grade of controls, sample size, age and gender were possible causes of heterogeneity. Taken together, our findings indicate that bevacizumab-induced hypertension can predict progress-free survival and overall survival in patients with metastatic colorectal cancer, whereas its prediction for objective response rate was nonsignificant.

Inhibition of the oxidative stress-induced miR-125b protects glucose metabolic disorders of human retinal pigment epithelium (RPE) cells.

The dysfunction of retinal pigment epithelium (RPE) with aging leads to age-related macular degeneration (AMD). Oxidative stress has been demonstrated as one of the causes of retinal pathological conditions. This study was conducted to investigate the mechanism of hydrogen peroxide (H2O2) induced human retinal pigment epithelial (RPE) cell dysfunction. We report miR-125b is induced by H2O2 treatments in RPE cells. In addition, we observed inhibited glucose metabolism under oxidative stress. Overexpression of miR-125b promotes the disorders of cellular glucose metabolism through direct targeting Hexokinase 2 (HK2). Restoration of HK2 in H2O2 treated RPE cells prevents the oxidative stress-suppressed glucose metabolism. Inhibition of the H2O2-induced miR-125b by inhibitor significantly prevented disorders of glucose metabolism. This study will contribute to the development of the miRNA based therapeutic approaches for against the oxidative stress-mediated human AMD.