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Non-responsiveness to immune-checkpoint blockade can result from limited T cell infiltration, mediated by the cells of the tumour microenvironment. Myofibroblastic cancer-associated fibroblasts (myoCAF)-rich tumours generally contain few T-cells and respond poorly to immune-checkpoint blockade. Although myoCAF are associated with poor outcome in most solid tumours, the molecular mechanisms regulating myoCAF accumulation remain unclear, limiting potential for therapeutic intervention.
The potential to target the myoCAF in combination with checkpoint inhibition in CAF-rich tumours could be a valid therapeutic startegy
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