Haoqiang Ying

TL;DR: In vivo mechanistic insights are provided into how oncogenic Kras promotes metabolic reprogramming in native tumors and illuminates potential metabolic targets that can be exploited for therapeutic benefit in PDAC.

TL;DR: The identification of a non-canonical pathway of glutamine use in human pancreatic ductal adenocarcinoma (PDAC) cells is reported and it is established that the reprogramming of glutamines metabolism is mediated by oncogenic KRAS, the signature genetic alteration in PDAC, through the transcriptional upregulation and repression of key metabolic enzymes in this pathway.

TL;DR: Inhibition of autophagy by genetic means or chloroquine treatment leads to robust tumor regression and prolonged survival in pancreatic cancer xenografts and genetic mouse models, and drugs that inactivate this process may have a unique clinical utility in treating pancreatic cancers and other malignancies with a similar dependence on Autophagy.

TL;DR: The path to meaningful clinical progress has never been clearer to improve PDAC patient survival and a deeper understanding of cancer cell biology, particularly altered cancer cell metabolism and impaired DNA repair processes, is providing novel therapeutic strategies that show strong preclinical activity.

TL;DR: It is demonstrated that a subpopulation of dormant tumour cells surviving oncogene ablation (surviving cells) and responsible for tumour relapse has features of cancer stem cells and relies on oxidative phosphorylation for survival.