Douglas E. Biancur

TL;DR: The results demonstrate a novel metabolic interaction between PSCs and cancer cells, in which PSC-derived alanine acts as an alternative carbon source and highlights a previously unappreciated metabolic network within pancreatic tumours in which diverse fuel sources are used to promote growth in an austere tumour microenvironment.

TL;DR: It is shown that, in PDAC, MHC-I molecules are selectively targeted for lysosomal degradation by an autophagy-dependent mechanism that involves theAutophagy cargo receptor NBR1 and leads to improved antigen presentation, enhanced anti-tumour T cell responses and reduced tumour growth in syngeneic host mice.

TL;DR: It is demonstrated that direct association via a key surface arginine in FTH1 and a C-terminal element in NCOA4 is required for delivery of ferritin to the lysosome via autophagosomes, explaining how intracellular iron levels modulate N COA4-mediated ferrit in cells and in an iron-dependent physiological setting.

TL;DR: This work demonstrates that autophagy is critical pancreatic tumor maintenance through tumor cell-intrinsic and -extrinsics mechanisms and illustrates the importance of assessing complex biological processes in relevant autochthonous models.

TL;DR: It is shown that despite marked early effects on in vitro proliferation caused by GLS inhibition, pancreatic cancer cells have adaptive metabolic networks that sustain proliferation in vitro and in vivo.