Fig. 4: Current treatments related to CAFs.
From: Cancer-associated fibroblasts in pancreatic ductal adenocarcinoma
(1) ECM and CAF depletion. Degrade key components of PDAC fibrosis, such as collagen and hyaluronic acid, or ablate specific CAFs subpopulations alone to prevent PDAC desmoplasia. (2) Deactivate or reprogram tumour-promoting CAFs into normalised fibroblasts in order to improve the tumour microenvironment. In some trials, iCAFs are converted to myCAFs to curb tumour progression. (3) Target key cytokines and chemokines and block related signalling in the crosstalk between CAFs, tumour cells, and immune cells, such as FAK signalling, the CXCL12-CXCR4 axis, and TGF-β signalling.
