ABSTRACT
Interactions of carcinogenic trace elements with cells and organisms include effector-type intersections with signal transduction pathways (STPs). An understanding of the relationships between these intersections and cellular, physiological, and genetic responses to metals is necessary to define adequately the extent to which metal-induced alterations in proliferation, apoptosis, differentiation, DNA repair, or metabolism of other xenobiotics contribute to metal-induced carcinogenesis. Such effects may complement direct mutagenic and clastogenic actions of the metal, or in some instances may represent the salient mechanisms by which the metal contributes to tumor formation and progression.
