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Abstract

This cancer cell-intrinsic GOT2-PPARδ axis promotes spatial restriction of both CD4+ and CD8+ T cells from the tumor microenvironment, and fosters the immune-suppressive phenotype of tumor-infiltrating myeloid cells. The immune-suppressive pathophysiology of PDAC has been linked to poor patient prognosis and makes most PDAC patients unresponsive to immune-therapies which have proven highly effective in cancers with improved T cell penetrance. Our results suggest that the GOT2-PPARδ axis could be a key player in the development of this immunological hallmark of PDAC.

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