Table 1.
Disease Model | Subtype | Features | Reference |
---|---|---|---|
Breast Cancer | vCAF | Derived from cells in the perivascular location. Express PDGFR-α. Produce high levels of α-SMA. | Bartoschek et al. [40] Sebastien et al. [42] |
cCAF | Similar to vCAF, except high expression of Ki67 and cell cycle genes. Thought to be vCAFs that are proliferative. | ||
mCAF | Derived from resident fibroblasts. Express PDGFR-β. Gene signatures for ECM activation and EMT observed. | ||
dCAF | Derived from epithelial tumor cells. Express genes related to tumor initiating cells. | ||
apCAF | Express MHCII but no other co-stimulatory molecules. Also express CD74. Can activate CD4+ T cells in an antigen-specific fashion. | Sebastien et al. [42] | |
Pancreatic Ductal Adenocarcinoma | myCAF | Derived from pancreatic stem cells and bone marrow-derived mesenchymal stem cells. Reside close to bulk of the primary tumor. Express PDGFR-α and α-SMA similar to vCAFs identified in breast cancer. | Ohlund et al. [43] |
iCAF | Secrete inflammatory cytokines. Reside far from the tumor, possibly originating from resident fibroblasts. Express PDGFR-β similar to mCAFs identified in breast cancer. | ||
apCAF | Similar to breast cancer apCAFs described above. | Elyada et al. [44] |