pancreatic ductal adenocarcinoma

[Free Radical Biology and Medicine] Scientists chose a panel of PDAC cell lines with diverse sensitivity to cisplatin and gemcitabine. In PANC-1 chemoresistant cells, they found a low level of oxidative stress and high levels of Nrf2 and YAP protein expressions and their respective targets.

[Medical Oncology] Researchers calculated IC50 of valproic acid -induced PANC-1 cells by combined analyses of proliferation and apoptosis, while assessing its effect on Wnt signaling pathway.

[Nature Reviews Gastroenterology & Hepatology] The authors describe the molecular machinery of cell death, discuss the complexity and multifaceted nature of lethal signalling in pancreatic ductal adenocarcinoma cells, and highlight the challenges and opportunities for activating cell death pathways through precision oncology treatments.

[Proceedings of the National Academy of Sciences of the United States of America] Researchers identified an important role for uridine diphosphate-glucose pyrophosphorylase 2 in the maintenance of pancreatic ductal adenocarcinoma growth in both in vitro and in vivo tumor models.

[Molecular Cancer Research] Researchers functionally studied candidate proteins using human normal and cancerous pancreatic ductal epithelial cell lines. 10-22 cell-derived pancreatic ductal adenocarcinoma (PDAC) displayed the molecular signature of clinical human PDAC.

[Nature Communications] Scientists employed an RNAi-based in vivo functional genomics platform to determine epigenetic vulnerabilities across a panel of patient-derived pancreatic ductal adenocarcinoma models.