V. T. Garrido

Combined MEK and STAT3 inhibition reprograms stromal inflammation to overcome immunotherapy resistance in pancreatic cancer

This paper shows that combining MEK and STAT3 inhibitors reprograms stromal inflammation and enhances immunotherapy response in pancreatic cancer.

Diet induced hyperlipidemia confers resistance to standard therapy in pancreatic cancer by selecting for "tumor protective" microbial metabolites and treatment refractory cells.

This study shows that a high-fat diet in pancreatic cancer mice increases resistance to chemotherapy by promoting microbial metabolites like queuosine, which protect tumors through PRDX1 upregulation, and this resistance can be reversed by S-adenosyl methionine.

Stroma secreted IL6 selects for stem-like population and alters pancreatic tumor microenvironment by reprogramming metabolic pathways

This study shows that stromal IL6 promotes stem-like cells and metabolic reprogramming in pancreatic tumors, creating an immune-evasive microenvironment that can be targeted to improve checkpoint inhibitor therapy.

Hypoxia driven oncometabolite L-2HG maintains "stemness"-differentiation balance and facilitates immune suppression in pancreatic cancer

This study shows hypoxia drives L-2HG production in pancreatic tumors, maintaining stemness-differentiation balance and promoting immune suppression, with LDH inhibition reversing these effects.

Targeting tumor intrinsic metabolic node in pancreatic cancer causes tumor regression, remodels extracellular matrix and sensitizes to anti-PD1 therapy.

This study shows that targeting the HBP metabolic node in pancreatic cancer with DON reduces tumor growth, remodels the ECM, and enhances response to anti-PD1 therapy.