Tumors and Tumor-Like Lesions of the Hepatobiliary Tract pp 1997-2017 | Cite as
Pathogenic Features of Liver Metastasis: Mechanisms Involving Platelets, Tumor Stroma, Epithelial-Mesenchymal Transition, and the Premetastatic Niche
Abstract
Homing of circulating cells to pre-metastatic niches of the liver and their subsequent growth to a metastasis requires a complex interaction between tumor cells and various normal cellular and matrix components of the future metastatic site. In the course of homing to endothelial surfaces of hepatic blood vessels and vascular invasion, tumor cells interact with platelets and induce platelet adhesion and aggregation. Tumor cell-induced thrombocyte aggregation facilitates early steps of metastasis through increased tumor cell arrest and formation of tumor cell emboli. Platelets participating in tumor cell aggregates promote cell adhesion and invasion and release growth factors for cancer cells. Following their exit from blood vessels, tumor cells engage in complex interactions with stromal cells. The stromal microenvironment profoundly influences growth and invasion of tumor cells in the metastatic site. Stromal cells interacting with tumor cells include cancer-associated fibroblasts and myofibroblasts, vascular cells, tumor-associated macrophages/TAMs, myeloid suppressor cells, and other cells of local immune responses. Cancer cells in turn constantly modulate the cellular composition of stroma, promote angiogenesis, and are subject to epithelial-mesenchymal transition.
Keywords
Cancer Stem Cell Premetastatic Niche Thrombocyte Aggregation Tumor Cell Embolus Streaming BloodReferences
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