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Intracellular signal transduction of cells in response to carcinogenic metals.
Crit Rec Oncol Hematol 2002 Apr; 42(1):105-121
Epidemiological and animal studies suggest that several metals and metal-containing compounds are potent mutagens and carcinogens. These metals include chromium, arsenic, vanadium, nickel, and others. During the last two decades, chemical and cellular studies have contributed enormously to our understanding of the mechanisms of metal-induced pathophysiological processes. Although each of these metals is unique in its mechanism of action, some common signaling molecules, such as reactive oxygen species (ROS), may be shared by many of the carcinogenic metals. New techniques are now available to reveal the mechanisms of carcinogenesis in precise molecular terms. In this review, we focused our attentions on carcinogenic metal-induced signal transduction pathways leading to the activation of NF-kappaB, cell apoptosis and cell cycle progression, three crucial steps or events involved in the transformation and carcinogenesis. This review summarizes current knowledge and our recent studies concerning intracellular signal transduction pathways initiated by carcinogenic metals and the cross-talk that occurs among these pathways in cells in response to metals.
Animal-studies; Cell-alteration; Cell-growth; Metal-compounds; In-vivo-studies; In-vitro-studies; Cell-transformation; Genes
Pathology and Physiology Research Branch, Health Effects Laboratory Division, National Institute for Occupational Safety and Health, 1095 Willowdale Road, Morgantown, WV 26505
7440-47-3; 1327-53-3; 7440-48-4; 7440-50-8; 7440-02-0; 1314-34-7; 7440-38-2; 1333-82-0; 1314-62-1
Issue of Publication
Research Tools and Approaches: Cancer Research Methods
Critical Reviews in Oncology Hematology
Page last reviewed: April 12, 2019
Content source: National Institute for Occupational Safety and Health Education and Information Division