Hsiang-Tsui Wang

Abstract It has long been recognized that non-muscle-invasive bladder cancer (NMIBC) has a low propensity (20%) of becoming muscle-invasive (MIBC), and that MIBC carry many more p53 point mutations (p53m) than NMIBC (50% vs 10%). MIBC also has a higher mutation burden than NMIBC. These results suggest that DNA repair capacities, mutational susceptibility and p53m are crucial for MIBC development.

Abstract Abnormal accumulation of acrolein, an α, β unsaturated aldehyde has been reported as one pathological cause of the CNS neurodegenerative diseases. In the present study, the neuroprotective effect of selumetinib (a MEK–ERK inhibitor) on acrolein-induced neurotoxicity was investigated in vitro using primary cultured cortical neurons. Incubation of acrolein consistently increased phosphorylated ERK levels. Co-treatment of selumetinib blocked acrolein-induced ERK phosphorylation.

Correction to: Scientific Reports https://doi.org/10.1038/s41598-019-38676-7, published online 21 February 2019 This Article contains errors in Figure 2 and the accompanying Figure legend. In panel C, in the bar graph showing Relative protein intensity (arbitrary units) for pEGFR, an asterisk (*) is incorrectly shown in the third bar. In panel D, the representative blot of pAKT is incorrect. Additionally, a representative blot for AKT is incorrectly shown.