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Pancreatic ductal adenocarcinoma (PDAC) is an aggressive disease in urgent need of improved therapy. A characteristic feature of PDAC is an abundant fibroinflammatory reaction that contributes to the treatment recalcitrancy of this disease. Here, tumour cells coinhabit a stiff, densely remodelled extracellular matrix (ECM) with abundant cancer-associated fibroblasts, immunosuppressive myeloid cell populations and regulatory T-cells that synergise to drive a CD8 T-cell-excluded tumour microenvironment (TME).1 The immune-deserted TME, in combination with a low neoantigen burden, is considered a major reason for the poor response to immune checkpoint inhibitors in PDAC.
While several studies have established that a remodelled ECM drives immune exclusion,2 the link between tissue stiffening and tumour cell autonomous mechanisms of immune evasion is less well explored. In a recent study, Canel and coworkers3 uncover a new mechanistic link between the scaffolding function of focal adhesion kinase (FAK) and PDAC immune escape (figure 1).
Contributors AB-G conceived and wrote the commentary and made the figure. CJ conceived and cowrote the commentary.
Funding Work in systems oncology is supported by a Cancer Research UK Institute Award (C5759/A27412), a Cancer Research UK Programme Award (C13329/A21671) and a European Research Council Consolidator Award (ERC-2017-CoG 772577).
Competing interests None declared.
Provenance and peer review Commissioned; internally peer reviewed.