Cancer Research | Tumor Fibrosis Biomarkers | Immune Checkpoint Inhibitor Therapy

Today Christina presents how tumor fibrosis and collagen fragments can be used in cancer research as biomarkers that can guide immune checkpoint inhibitor therapy.
There is an unmet medical need for predictive biomarkers that can guide patient selection and treatment decisions. Emerging evidence indicates that one central common denominator of resistance to immune checkpoint inhibitors may be fibrotic activity characterized by collagen production by cancer-associated fibroblasts (CAFs).
Consequent to increased fibroblast activity, specific collagen fragments are released into the circulation and can be used as non-invasive biomarkers assessed in a liquid biopsy such as serum or plasma. PRO-C3 quantifies the formation of type III collagen and can therefore be used as a non-invasive biomarker of tumor fibrosis.
As demonstrated here, high levels of PRO-C3 in serum were associated with poor overall survival in patients with metastatic melanoma treated with immune checkpoint inhibitors. The same applies to other solid tumor types indicating that this assay is indeed relevant for immuno-oncology.
C4G is a serum biomarker that quantifies granzyme B mediated degradation of type IV collagen. Granzyme B promotes T cell infiltration
through the basement membrane by degradation of type IV collagen. High levels of C4G are found to identify metastatic melanoma patients that do respond to immune checkpoint inhibitor treatment.
Furthermore, in a pre-clinical study with the T cell engager NC410 that induces T cell activity, it was observed that C4G levels were increased at the time of tumor eradication in treated mice, while C4G remained low
in untreated mice supporting C4G is a non-invasive biomarker for T-cell activity and infiltration.
Therefore, these data indicate that PRO-C3 ​and C4G as serum biomarkers can be applied as a non-invasive biomarker tool for patients undergoing immune checkpoint inhibitor therapy.
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