Jinyang Li

TL;DR: A library of congenic tumor cell clones from an autochthonous mouse model of pancreatic adenocarcinoma is established, identifying heterogeneous and multifactorial pathways regulating tumor‐cell‐intrinsic mechanisms that dictate the immune microenvironment and thereby responses to immunotherapy.

TL;DR: Using a lineage-labeled mouse model of pancreatic ductal adenocarcinoma to study EMT in vivo, it is found that most tumors lose their epithelial phenotype through an alternative program involving protein internalization rather than transcriptional repression, resulting in a "partial EMT" phenotype.

TL;DR: In PDAC models, therapy-induced senescence can establish emergent susceptibilities to otherwise ineffective chemo- and immunotherapies through SASP-dependent effects on the tumor vasculature and immune system.

TL;DR: In this article, the effect of blocking CA9, in combination with administration of gemcitabine, in mouse models of pancreatic cancer, was evaluated in the presence of hypoxia and dysplasticity.

TL;DR: The findings warrant clinical trials testing the effectiveness of therapies combining EPHA2-TGFβ-PTGS2 pathway inhibitors with anti-tumor immunotherapy, and may change the treatment of notoriously therapy-resistant pancreatic adenocarcinoma.