K. Kesh

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.

Microbial Dysbiosis and polyamine metabolism as predictive markers for early detection during progression of pancreatic adenocarcinoma in spontaneous mouse model

Long non-coding RNA GAS5 acts as proliferation brakes in CD133+ cells responsible for tumor recurrence

This study shows GAS5 regulates quiescence and growth arrest in CD133+ cells, which drive tumor recurrence in pancreatic cancer by inhibiting cell cycle progression and altering metabolic pathways.

O-GlcNAc modification of oncogenic transcription factor Sox2 promotes protein stability and regulates self-renewal in pancreatic cancer

This study shows that O-GlcNAc modification of Sox2 stabilizes the protein and enhances self-renewal in pancreatic cancer, with targeting OGT reducing tumor burden.