Endothelial dysfunction is recognized to contribute to chronic tissue remodeling in the lung, yet endothelial-derived mechanisms driving these processes remain largely undefined. Here, we show that endothelial inactivation of the LATS1 and LATS2 kinases, key suppressors of the transcriptional regulators YAP and TAZ, el...
K. Kontodimas, A. Raslan, Benjamin Spira et al.· Science Advances· 0 citations
Purpose A minority of patients with bladder cancer derive lasting benefit from immunotherapy, and current biomarkers capture only part of the biology. We evaluated whether tumor-cell MHC class II defines an immune state associated with outcome across disease stages and after PD-1/PD-L1 blockade. Experimental Design We...
J. Bellmunt, Ying-Tian Xie, M. Munoz et al.· bioRxiv· 0 citations
Phenotypic plasticity is a recognized mechanism of therapeutic resistance in prostate cancer (PCa); however, current knowledge of its underlying drivers and therapeutic interventions remain limited. Using genetically engineered mouse models (GEMMs) devoid of Pten and Rb1, we previously demonstrated the chromatin reprog...
Beatriz German, K. Morel, Teia Noel et al.· Cell Reports Medicine· 0 citations
In vitro co-culture assays using ACKR1+ VECs isolated from IPF lungs demonstrate that these cells drive myeloid recruitment and fibroblast activation through ACKR1 dependent mechanisms and show that pharmacologic inhibition of ACKR1 attenuates experimental lung fibrosis.
K. Kontodimas, A. Raslan, Benjamin Spira et al.· bioRxiv· 0 citations
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