CAV1-DOT1L axis in TAM-derived EVs orchestrates VM and sensitises PDAC to combined VM and VEGF targeting
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The authors investigate the regulatory mechanisms of vasculogenic mimicry (VM) in pancreatic ductal adenocarcinoma (PDAC) and explore therapeutic strategies to counteract VM-driven tumor progression. They identify a CAV1-DOT1L-ATG5 axis in tumor-associated macrophage (TAM)-derived extracellular vesicles that promotes VM, and demonstrate that combined inhibition of DOT1L and VEGF receptor (VEGFR) effectively targets both VM and compensatory angiogenesis, offering a promising approach for PDAC treatment.
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