Taiji Yamazoe

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: 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.

TL;DR: Using a K-to-M histone mutant to directly inhibit H3K36me2, it is found that global modulation of the mark is a conserved mechanism underlying the mesenchymal state in various contexts.

TL;DR: Examination of the role of the ubiquitin-specific protease 22 (USP22) as a regulator of the immune tumor microenvironment (TME) in PDA indicated that USP22 regulates immune infiltration and immunotherapy sensitivity in preclinical models of pancreatic cancer.