Tumor-associated collagen (TAC)

Tumor-associated collagen refers to the remodeled and often overexpressed collagenous components of the extracellular matrix (ECM) within the tumor microenvironment [1]. In many solid tumors, particularly pancreatic and breast cancers, a desmoplastic response leads to the accumulation of dense, linearized fibrillar collagens (primarily Type I and III) that create a physical barrier against immune cell infiltration and drug penetration [2][3]. Beyond its structural role, tumor-associated collagen actively promotes cancer progression by activating signaling pathways such as integrins and discoidin domain receptors (DDRs), which drive cell proliferation, survival, and epithelial-to-mesenchymal transition (EMT) [4]. Therapeutically, this collagen is targeted through two primary strategies: direct degradation or inhibition of its synthesis to normalize the stroma, and utilizing its high density as a docking station for drugs fused to collagen-binding domains (CBDs) to improve local retention and reduce systemic toxicity [5][6]. Monitoring collagen organization, such as through Tumor-Associated Collagen Signatures (TACS), provides significant prognostic value regarding patient survival and metastatic risk [7]. Sources: [1] Fang et al. (2014) Cancer Microenviron; [2] Provenzano et al. (2006) BMC Med; [3] Wegner et al. (2020) Front Oncol; [4] Shintani et al. (2008) J Cell Biol; [5] Ishihara et al. (2017) Sci Transl Med; [6] Mpekris et al. (2017) Cancer Res; [7] Conklin et al. (2011) Am J Pathol.

Other names

Tumor-associated collagen signaturesTACSCancer-associated collagenDesmoplastic collagenFibrillar collagen

Inhibition of collagen synthesis, enzymatic collagen degradation, and collagen-binding mediated drug localization