Selenium (Se) was recognized to be an essential trace element in humans and animals in the late 1950s. A decade later, anticarcinogenesis was suggested by statistical correlation of decreased cancer mortality with increased Se in the diet in the United States (71). Scientific evidence indicates that indeed Se plays a role in cancer prevention (72-76). Se was shown to inhibit growth and to stimulate programmed cell death in a variety of cell culture studies, including human tumor cell lines in vitro (77). Hundreds of animal studies demonstrate that Se can reduce tumor yields: moderate Se supplementation at levels above the dietary requirements has been shown to decrease the number of tumors induced by several chemical carcinogens and viruses and to reduce the incidence of spontaneous mammary tumors (78) as well as the growth of other transplanted tumors (78).
Some, but not all, epidemiological studies have found a reduced risk for several kinds of cancer associated with a higher blood concentration of Se (79,80). A decreased Se concentration and glutathionine peroxidase (GPX) activity in blood and, interestingly, an increase of these parameters in malignant tissue was found in lung cancer patients (80). An initial study of 240 non-melanoma skin cancer patients in good general health demonstrated a significantly lower mean plasma Se concentration than control subjects without skin cancer (81). In fact, those patients whose blood concentrations were in the lowest decile had 4.4 times the incidence of skin cancer as those in the highest decile (81).
In a 10-year prospective study of 1312 patients with a history of basal cell or squamous cell carcinomas of the skin, Se treatment did not protect against further development of such skin cancers; however, it did reduce total cancer incidence, total cancer deaths, and the incidence of lung, colorectal, prostate, and total non-skin cancer (82,83).