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Cancer cell invasion necessitates the participation of host cells. One of the cell types that stimulates invasion of colon and other cancer cells is the myofibroblast, as evidenced from the histology of cancer and from coculture experiments. Cancer cells produce transforming growth factor-β (TGF-β) and TGF-β converts fibroblasts into pro-invasive myofibroblasts. In the in vitro system with human cancer cell lines and freshly isolated stromal cells, the pro-invasive activity of myofibroblasts is due to the combined action of Hepatocyte growth factor/scatter factor (HGF/SF) and tenascin-C, two molecules known to promote invasion in clinical tumors and their experimental surrogates. The myofibroblasts are themselves invasive and this activity is stimulated by TGF-β. N-cadherin is implicated in the invasion response of myofibroblasts. The question now is which of the multiple factors present in the tumor ecosystem is responsible for the pro-invasive switch that turns a benign tumor into a malignant one.

Cancer cell invasion necessitates the participation of host cells. One of the cell types that stimulates invasion of colon and other cancer cells is the myofibroblast, as evidenced from the histology of cancer and from coculture experiments. Cancer cells produce transforming growth factor-β (TGF-β) and TGF-β converts fibroblasts into pro-invasive myofibroblasts. In the in vitro system with human cancer cell lines and freshly isolated stromal cells, the pro-invasive activity of myofibroblasts is due to the combined action of Hepatocyte growth factor/scatter factor (HGF/SF) and tenascin-C, two molecules known to promote invasion in clinical tumors and their experimental surrogates. The myofibroblasts are themselves invasive and this activity is stimulated by TGF-β. N-cadherin is implicated in the invasion response of myofibroblasts. The question now is which of the multiple factors present in the tumor ecosystem is responsible for the pro-invasive switch that turns a benign tumor into a malignant one.

Cancer cell invasion necessitates the participation of host cells. One of the cell types that stimulates invasion of colon and other cancer cells is the myofibroblast, as evidenced from the histology of cancer and from coculture experiments. Cancer cells produce transforming growth factor-β (TGF-β) and TGF-β converts fibroblasts into pro-invasive myofibroblasts. In the in vitro system with human cancer cell lines and freshly isolated stromal cells, the pro-invasive activity of myofibroblasts is due to the combined action of Hepatocyte growth factor/scatter factor (HGF/SF) and tenascin-C, two molecules known to promote invasion in clinical tumors and their experimental surrogates. The myofibroblasts are themselves invasive and this activity is stimulated by TGF-β. N-cadherin is implicated in the invasion response of myofibroblasts. The question now is which of the multiple factors present in the tumor ecosystem is responsible for the pro-invasive switch that turns a benign tumor into a malignant one.

Cancer cell invasion necessitates the participation of host cells. One of the cell types that stimulates invasion of colon and other cancer cells is the myofibroblast, as evidenced from the histology of cancer and from coculture experiments. Cancer cells produce transforming growth factor-β (TGF-β) and TGF-β converts fibroblasts into pro-invasive myofibroblasts. In the in vitro system with human cancer cell lines and freshly isolated stromal cells, the pro-invasive activity of myofibroblasts is due to the combined action of Hepatocyte growth factor/scatter factor (HGF/SF) and tenascin-C, two molecules known to promote invasion in clinical tumors and their experimental surrogates. The myofibroblasts are themselves invasive and this activity is stimulated by TGF-β. N-cadherin is implicated in the invasion response of myofibroblasts. The question now is which of the multiple factors present in the tumor ecosystem is responsible for the pro-invasive switch that turns a benign tumor into a malignant one.