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From the Departments of Pediatrics and Biochemistry and Molecular Biology,* University of Southern California Keck School of Medicine and The Saban Research Institute of Childrens Hospital Los Angeles, Los Angeles, California; the Department of Pathology, Beth Israel Deaconess Medical Center, Boston, Massachusetts; the Department of Cell and Molecular Biology, Northwestern University Medical School, Chicago, Illinois; the Department of Medicine, University of California San Francisco School of Medicine, San Francisco, California; the Department of Cellular and Molecular Pathology,¶ Vanderbilt University School of Medicine, Nashville, Tennessee; the Department of Pathology and Laboratory Medicine,|| University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania; the Departments of Pathology and Radiation Oncology,** Karmanos Cancer Institute, Wayne State University School of Medicine, Detroit, Michigan; the Department of Cancer Biology, Vanderbilt University School of Medicine, Nashville, Tennessee; the Department of Pharmacology, Wayne State University School of Medicine, Detroit, Michigan; the Department of Tumor and Development Biology, University of Liege, Liege, Belgium; the Department of Anatomy and Cell Biology,¶¶ Holden Comprehensive Cancer Center, University of Iowa, Iowa City, Iowa; the Cancer Research Institute and Department of Pathology,|||| University of California San Francisco School of Medicine, San Francisco, California; and the Center for Scientific Review,*** National Institutes of Health, Bethesda, Maryland
Abstract
The role of the extracellular matrix (ECM) in the tumor microenvironment is not limited to being a barrier against tumor invasion. The ECM is a reservoir of cell binding proteins and growth factors that affect tumor cell behavior. It is also substantially modified by proteases produced by tumor cells or stroma cells. As a result of the activity of these proteases, cell-cell and cell-ECM interactions are altered, new biologically active ECM molecules are generated, and the bioavailability and activity of many growth factors, growth factor receptors, and cytokines are modified. ECM-degrading proteases also play a critical role in angiogenesis, where they can act as positive as well as negative regulators of endothelial cell proliferation and vascular morphogenesis. This review article summarizes some of the most relevant findings made over the recent years that were discussed at a workshop organized by the Path B Study Section of the National Institutes of Health in October 2002.
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