Mounting evidence reveals that selenium is a dietary constituent with anticarcinogenic and antitumorigenic properties. Various forms of selenium appear to be effective in bringing about these effects, although preclinical studies suggest that differences may arise as the quantity provided is reduced. The literature also documents the greater sensitivity of neoplastic cells to selenium than their nonneoplastic counterparts. Unfortunately, the minimal amount needed to bring about a positive effect in humans remains elusive. If there is a positive response to exaggerated intakes, it will likely be dependent on many factors, including the consumption of other dietary constituents, as well as variation in a host of genetic pathways involved with cancer. Although the biological basis of the reduction in cancer risk ascribed to selenium remains to be established, its consistency in retarding various experimentally induced tumors and suppressing the growth of various types of neoplasms in vitro and in vivo suggests that several mechanisms are involved. Depressed carcinogen bioactivation, reduced cell proliferation, and increased apoptosis raise the possibility that selenium works at a number of specific molecular targets involved with the cancer process. This review will focus on molecular targets involved with cell proliferation and apoptosis as possible mechanisms by which selenium might alter the cancer process.