Jithesh J. Augustine

TL;DR: A widely prevalent mechanism of resistance to gemcitabine in pancreatic cancer is established, whereby increased glycolytic flux leads to glucose addiction in cancer cells and a corresponding increase in pyrimidine biosynthesis to enhance the intrinsic levels of deoxycytidine triphosphate (dCTP).

TL;DR: In this article, the authors identify a cooperative node between oncogenic KRAS effectors and mutant p53 that can be therapeutically targeted to undermine cooperation and mitigate metastasis, and they show that CREB1 inhibition dramatically reduced FOXA1 and β-catenin expression and dampened PDAC metastasis.

TL;DR: This study proposes that activation of GPER1 may constitute a new avenue for pancreatic cancer therapeutics, and indicates activation of G‐protein‐coupled estrogen receptor (GPER1) as the main underlying mechanism of action.

TL;DR: It is demonstrated that auranofin prevents pancreatic ductal adenocarcinoma progression using multiple models and suggests inhibition of Txnrd1 and HIF-1α as possible mechanisms of action, and TxNrd1 as a biomarker of resistance.