Table 1. Relative Risk (RR) Related to Family History of Prostate Cancera continued...
Other nutrients have been studied for their potential influence on prostate cancer risk. The effect of selenium and vitamin E in preventing prostate cancer was studied in the Selenium and Vitamin E Cancer Prevention Trial (SELECT). This randomized placebo-controlled trial of selenium and vitamin E among 35,533 healthy men found no evidence of a reduction in prostate cancer risk, although a statistically significant increase (HR, 1.17; 99% CI, 1.004–1.36; P = .008) in prostate cancer with vitamin E supplementation alone was observed. The absolute increased risk associated with vitamin E supplementation compared to placebo after more than 7 years of follow-up was 1.6 per 1,000 person years.
(Refer to the PDQ summary on Prevention of Prostate Cancer for more information about risk factors for prostate cancer in the general population.)
The Surveillance, Epidemiology and End Result Cancer Registries has assessed the risk of developing a second primary cancer in 292,029 men diagnosed with prostate cancer between 1973 and 2000. Excluding subsequent prostate cancer and adjusting for the risk of death from other causes, the cumulative incidence of a second primary cancer among all patients was 15.2% at 25 years (95% CI, 5.01–5.4). There was a significant risk of new malignancies (all cancers combined) among men diagnosed prior to age 50 years, no excess or deficit in cancer risk in men aged 50 to 59 years, and a deficit in cancer risk in all older age groups. The authors suggested that this deficit may be attributable to decreased cancer surveillance in an elderly population. Excess risks of second primary cancers included cancers of the small intestine, soft tissue, bladder, thyroid, and thymus, and melanoma. Prostate cancer diagnosed in patients aged 50 years or younger was associated with an excess risk of pancreatic cancer.
The underlying etiology of developing a second primary cancer after prostate cancer may be related to various factors. Some of the observed excess risks could be associated with prior radiation therapy. Radiation therapy as the initial treatment for prostate cancer was found to increase the risk of bladder and rectal cancers and cancer of the soft tissues. More than 50% of the small intestine tumors were carcinoid malignancies, suggesting possible hormonal influences. The excess of pancreatic cancer may be due to mutations in BRCA2, which predisposes to both. The risk of melanoma was most pronounced in the first year of follow-up after diagnosis, raising the possibility that this is the result of increased screening and surveillance.
One Swedish study using the nationwide Swedish Family Cancer Database assessed the role of family history in the risk of a second primary cancer following prostate cancer. Of 18,207 men with prostate cancer, 560 developed a second primary malignancy. Of those, the relative risk (RR) was increased for colorectal, kidney, bladder, and squamous cell skin cancers. Having a paternal family history of prostate cancer was associated with an increased risk of bladder cancer, myeloma, and squamous cell skin cancer. Among prostate cancer probands, those with a family history of colorectal cancer, bladder cancer, or chronic lymphoid leukemia were at increased risk of that specific cancer as a second primary cancer.