A new study suggests that excessive use of zinc supplements may be associated with an increased risk of prostate cancer.
Zinc is found in higher concentrations in the prostate than any other soft tissue in the body, and studies have suggested that high concentrations of zinc in the prostate may have a negative effect on risk of prostate cancer. In the United States, 10% of men who take zinc supplements take 2 to 3 times more than the recommended dietary allowance of 11 mg per day.
Michael F. Leitzmann, M.D., of the National Cancer Institute and his colleagues examined zinc intake and prostate cancer risk among 46,974 U.S. men participating in the Health Professionals Follow-Up study. Compared with nonusers, men who consumed more than 100 mg/day of supplemental zinc had more than twice the risk of advanced prostate cancer. A similar increase in risk was seen among men who used supplemental zinc for 10 or more years. No association was seen between supplemental zinc intake of less than 100 mg/day and prostate cancer risk.
Contact: NCI Office of Communications, 301-496-6641, ncipressofficers@mail.nih.gov.
Study Finds No Association Between Presence of SV40 DNA and Lymphoma
A British study has found no evidence of simian virus 40 (SV40) DNA in non-Hodgkin's lymphoma (NHL) samples, challenging the theory that exposure to SV40-contaminated poliovirus vaccine in the 1950s and 1960s is associated with the development of NHL.
Jane MacKenzie, Ruth F. Jarrett, and their colleagues from the University of Glasgow in the United Kingdom, looked for the presence of SV40 DNA in 259 blood and tumor samples from patients in the U.K. with lymphadenopathy and lymphoid leukemia. The researchers did not detect SV40 DNA in any lymphoid sample examined. "Because the incidence of NHL is similar in the United Kingdom and the United States, this finding suggests that SV40 is unlikely to have an etiologic role in NHL," the researchers conclude.
Modified Prodrug Targets Prostate Cancer Cells
By modifying the natural plant compound thapsigargin so that it is activated only at metastatic sites, researchers have created a prodrug that selectively kills prostate tumor cells.
The discovery gets around one of the biggest problems with thapsigargin: its toxicity to both normal and cancerous cells. The compound works by disrupting intracellular calcium balance.
Samuel R. Denmeade, M.D., of the Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins and his colleagues coupled thapsigargin to a peptide that is activated when cleaved by prostate-specific antigen (PSA), an enzyme that is produced specifically by prostate cancer cells. Transplanted human prostate tumors stopped growing in mice treated with the prodrug, and there was no substantial host toxicity. The authors note that this approach is being developed for testing in clinical trials as a treatment for metastatic prostate cancer.
Contact: Valerie Mehl, Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, 410-955-1287, mehlva@jhmi.edu.
Study Finds Overuse of Therapy for Localized Prostate Cancer
Androgen deprivation therapy, a treatment for advanced prostate cancer, is increasingly being used by men with localized prostate cancer, a new study has found. Yet the appropriateness of such therapy for localized prostate cancer remains unclear.
Matthew R. Cooperberg, M.D., Peter R. Carroll, M.D., and their colleagues at the University of California San Francisco, Mount Zion Comprehensive Cancer Center analyzed patterns of prostate cancer treatment between 1989 and 2001 and found a dramatic increase in the use of both primary and neoadjuvant androgen deprivation therapy use among patients in all risk groups (high, intermediate, and low) and in association with different treatments such as radical prostatectomy and radiation therapy.
The authors say that clinical trials are needed to better define the role of androgen deprivation therapy in localized prostate cancer and that the results of these trials should be used to update clinical guidelines.
Contact: Eve Harris, UCSF Comprehensive Cancer Center, 415-476-2557, eharris@pubaff.ucsf.edu.
Gene Mutation Predicts Prognosis in Non-Small-Cell Lung Cancer
Mutations in the p53 tumor suppressor gene are a predictor of poor prognosis in patients with non-small-cell lung cancer, according to a new study.
Steven A. Ahrendt, M.D., of the University of Rochester and his colleagues analyzed tumor samples from 188 patients with NSCLC for the presence of p53 mutations. They found that patients with p53 mutations in their tumors had a statistically significantly higher risk of death than patients with normal copies of the p53 gene. However, the prognostic role of p53 mutations appeared to be limited to patients with stage I NSCLC.
The researchers say that new drugs that specifically target cells overexpressing mutant p53 may be a promising approach to treating patients with stage I NSCLC. They say that additional studies of such targeted adjuvant therapy in this population is needed.
Contact: Leslie White, University of Rochester Medical Center, 585-273-1119, leslie_white@urmc.rochester.edu.
Note: The Journal of the National Cancer Institute is published by Oxford University Press and is not affiliated with the National Cancer Institute. Attribution to the Journal of the National Cancer Institute is requested in all news coverage.
Journal
JNCI Journal of the National Cancer Institute