title: New concepts in selenium chemoprevention.
abstract: This article highlights some recent advances in selenium cancer chemoprevention research. It has been well documented that the chemical transformation of selenium to a monomethylated metabolite is an important step in achieving cancer prevention. Studies with the rat mammary carcinogenesis model suggested that methylselenocysteine (MSC), a good precursor for generating methylselenol endogenously, is able to block clonal expansion of premalignant lesions in the mammary gland. This finding supports the notion that selenium intervenes at an early stage of carcinogenesis. In addition to decreasing cell proliferation of the transformed colonies in vivo, MSC also enhances apoptosis. These same cellular responses are replicated with human premalignant breast cells grown in culture. cDNA microarray analysis indicated that selenium affects a multitude of molecular targets. Based on this information, a number of signaling pathways are proposed that could potentially provide insight into how selenium might block cell cycle progression and induce cell death.
authors.affiliation: Department of Experimental Pathology, Roswell Park Cancer Institute, Buffalo, NY 14263, USA clement.ip@roswellpark.org
authors.forename: Clement
authors.initials: C
authors.lastname: Ip
authors.forename: Yan
authors.initials: Y
authors.lastname: Dong
authors.forename: Howard E
authors.initials: HE
authors.lastname: Ganther
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D002453:Cell Cycle / Q000187:drug effects; D006801:Humans; D009369:Neoplasms / Q000517:prevention & control*; D018036:Selenium Compounds / Q000494:pharmacology* / Q000627:therapeutic use
chemical_list: D018036:Selenium Compounds