An emerging theme in cancer biology is how, in addition to genetic alterations in signaling pathways (eg. MAPK and PI3K), cancer cells can hijack normal stress response pathways to overcome strict reliance on external nutrients for growth. Pancreatic ductal adenocarcinoma (PDA) is the quintessence of an aggressive malignancy that thrives in nutrient poor, hypoxic environments, by altering pathways responsible for nutrient acquisition and utilization, such as autophagy and macropinocytosis.
In our lab we study the mechanisms of autophagy-lysosome activation and how this organellar system contributes to metabolic reprogramming in PDA. We hypothesize that the functional interplay between cellular trafficking pathways and activation of gene programs that regulate organelle dynamics and function are tightly coupled and essential for tumor growth. Our studies at the intersection of cell biology and cancer research, using a combination of biochemistry, immuno-fluorescence imaging, proteomics and metabolomics in PDA cell lines, primary patient derived culture systems and genetically engineered mouse tumor models, aims to provide insight into how fundamental cellular process are rewired in cancer while also identifying new nodes for anti-cancer therapy.