Fazlul H. Sarkar

TL;DR: The inhibition of Akt and NF-kappaB activity and their cross-talk provide a novel mechanism by which genistein inhibits cell growth and induces apoptotic processes in tumorigenic but not in nontumorigenic prostate epithelial cells.

TL;DR: Pancreatic CC of the pancreas is associated with a significantly better prognosis than ordinary ductal adenocarcinoma and appears to have a low incidence of mutation in codon 12 of the k-ras gene, which may contribute to thromboembolic complications or even dissemination of the tumor.

TL;DR: The results suggest that the activation of Notch-1 signaling contributes to the acquisition of EMT phenotype, which is in part mediated through the regulation of miR-200b and CSC self-renewal capacity, and these processes could be attenuated by genistein treatment.

TL;DR: The results here support a dichotomy in the dysplasia–CIS sequence in the pancreas and support the previous impression that MUC2 (the mucin associated with gel formation) is a marker of the “indolent” pathway (intraductal papillary mucinous neoplasm and colloid carcinoma).

TL;DR: The role of Notch signaling pathway is described, and how its deregulation is involved in EMT and tumor aggressiveness is cataloged, which could become a novel approach for cancer prevention and treatment.