María Crespo, Barbara Gonzalez-Teran ... Guadalupe Sabio
Circadian neutrophil infiltration in the liver modulates liver clock-gene expression and daily hepatic metabolism through the secretion of elastase and activation of JNK-FGF21-Bmal1 axis in the hepatocyte.
In the absence of ROCK1 activation by caspases, apoptotic cells don’t undergo typical morphological changes, leading to sterile inflammation in the liver that increases tissue damage and suppresses tumor formation.
Circulating myeloid cells invade the brain during pancreatic cancer, where they accumulate at a unique central nervous system interface and drive anorexia and muscle catabolism.
Tissue-resident natural killer cells are important mediators of CD8 T responses in human cancers and these cells can be harnessed to increase immunity against pancreatic ductal adenocarcinoma.
Mutations in the gene for β-catenin cause liver cancer cells to release fewer exosomes, which reduces the number of immune cells infiltrating the tumor.
Renumathy Dhanasekaran, Virginie Baylot ... Dean W Felsher
MYC and Twist1 drive metastasis by a novel non-cell-autonomous transcriptional mechanism of eliciting a cytokinome that mediates the crosstalk between cancer cells and macrophages, and its therapeutic blockade inhibits metastasis.
Shikai Hu, Jacquelyn O Russell ... Satdarshan P Monga
Ductular reaction often observed in chronic liver pathologies such as in cystic fibrosis could be due to disruption of a novel complex of β-catenin-NF-κB and CFTR in cholangiocytes, which leads to persistent nuclear translocation of p65 and NF-κB activation.
Irini Papazian, Maria Kourouvani ... Lesley Probert
Severely immunodeficient B2m-NOG mice transplanted with human peripheral blood mononuclear cells from multiple sclerosis patients partially reproduce disease immunopathology and represent novel experimental models for studying human immune responses to the central nervous system in a rapid and personalized manner.
Resting natural killer cells promote the progress of colon cancer liver metastasis (CCLM), which may be exploited for novel strategies to improve therapeutic outcomes for patients with CCLM.
