Fig 1: Hypothetical illustration showing how the ECM-derived biomarkers may associate with cancer-immune phenotypes. (Left) During T-cell infiltration into the tumor microenvironment, T cells release granzyme B (GzB) to break down type IV collagen to pass through the basement membrane which may result in released fragments of granzyme B degraded type IV collagen (C4G) into the circulation. In the immune-inflamed phenotype, many of these T cells are positioned in the tumor parenchyma, while in the immune-excluded phenotype (Middle), the T cells are retained in the high-density collagen barrier that may release type III collagen fragments into the circulation (PRO-C3). (Right) In the immune-desert phenotype, few or no T cells are found in the tumor microenvironment.
Fig 2: Specificity of the C4G monoclonal antibody. The monoclonal antibody’s reactivity in the competitive C4G ECLIA was tested toward (A) the selection peptide (MGNTGPTGAV), an elongated peptide (FMGNTGPTGAV), a truncated peptide (GNTGPTGAV), a non-sense selection peptide (LLARDFEKNY), and a non-sense coating peptide (LLARDFEKNY-K-biotin) and (B) the selection peptide (MGNTGPTGAV) and the deselections peptide 1 (MGQTGPTGAV), 2 (MGNSGPTGAV), and 3 (QGNTGPTGAV). %B/B0: B equals the intensity of a sample well (OD at x ng/mL peptide) and B0 equals the maximum intensity (OD at 0 ng/mL peptide). (C) The a2 chain of type IV collagen was incubated for 24 h without or with the serine proteases granzyme B (GzB) or neutrophil elastase (NE), or the matrix metalloproteinases (MMPs) MMP-2 or MMP-9. The buffer added proteases alone were included as negative controls. Data is based on two independent experiments and presented with mean and standard deviation. The dotted line represents the lower limit of measurement.
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