© 2001 by Oxford University Press
Journal of the National Cancer Institute, Vol. 93, No. 3, 165,
February 7, 2001
© 2001 Oxford University Press
IN THIS ISSUE |
The use of cellular telephones has increased dramatically over the past few years. Few laboratory studies have provided evidence to support the biologic plausibility of increased cancer risk from exposure to radiofrequency radiation, but until recently, no studies in humans had addressed the question. Johansen et al. (p. 203) followed more than 420 000 Danish cell phone subscribers for the incidence of all cancers from 1982 to 1995. Compared with the Danish population at large, the authors found no excesses of cancer at any site, including three of a priori interest: brain or nervous system, leukemia, and salivary gland. The results did not vary according to age, length of cell phone use, or type of cell phone (digital or analog). The authors note that this is the first cancer incidence cohort study to date of the cellular phone and cancer issue.
In an editorial, Park (p. 166) discusses the history of the controversy surrounding nonionizing radiation and cancer risk and the media’s role in supporting public fears. He emphasizes that scientists have a responsibility to put relevant evidence into the proper perspective for the public.
"A beautifully designed, nationwide, epidemiologic study of cell phone use and cancer has been carried out in Denmark. . . . The large cohort and the rock-solid database make it difficult to take issue with the report’s conclusion."
—Park
bcl-2 Overexpression and Angiogenic Potential
Many tumors overexpress the bcl-2 oncogene, which promotes tumor growth by inhibiting hypoxia-induced apoptosis. Fernandez et al. (p. 208) tested the effects of bcl-2 overexpression in prostate carcinoma cell lines by measuring vascular endothelial growth factor (VEGF) expression in cells cultured in hypoxic (1% O2) or normoxic (19% O2) conditions and by analyzing the angiogenic potential of xenografts derived from the bcl-2-transfected cells. The authors found that, compared with control cells, prostate carcinoma cells overexpressing bcl-2 had higher levels of VEGF when they were cultured in hypoxic conditions and that in vivo xenograft tumors derived from bcl-2-overexpressing cells grew more aggressively and had increased angiogenic potential. The authors suggest that inhibiting bcl-2 expression in prostate tumors could inhibit angiogenesis in addition to resensitizing such tumors to hypoxia-induced apoptosis.
Epidermal Growth Factor and DNA Damage
Hamada et al. previously found that malignant changes occurring in the weakly malignant cell line ER-1 after a 24-hour exposure to epidermal growth factor (EGF) were reversible but after a 1-month exposure were irreversible. In this issue (p. 214), they assess these malignant changes by measuring intracellular peroxide levels, 8-hydroxydeoxyguanosine levels (a marker of DNA damage), invasiveness, tumorigenicity, and metastatic ability. After a 1-month exposure to EGF, treated cells had higher levels of intracellular peroxide and 8-hydroxydeoxyguanosine and were more tumorigenic, metastatic, and invasive than untreated cells. However, when N-acetylcysteine or selenium was added with EGF for 1 month, levels of intracellular peroxide and 8-hydroxydeoxyguanosine were comparable to those in control cells; tumorigenicity and metastatic ability were also diminished. The authors conclude that irreversible changes induced by a 1-month exposure to EGF were caused by oxidative damage to the DNA that could be inhibited by antioxidants.
Ethnic Background and Prostate Cancer Mortality
African-American men have a higher incidence of prostate cancer than white American men and are more likely to die of the disease. Earlier studies have suggested that this difference may reflect unequal access to health care, resulting in a later stage at diagnosis and, consequently, worse prognostic variables among African-Americans. It could also reflect ethnic differences in the biology of metastatic prostate cancer. To investigate this question, Thompson et al. (p. 219) analyzed survival differences by ethnicity in men with metastatic disease enrolled in a randomized phase III treatment trial. After adjustment for a number of prognostic variables—disease extent, bone pain, performance status, age, Gleason score, and prostate-specific antigen level—survival was still poorer among African-American men in the study. Adjustment for quality-of-life assessments also did not eliminate the survival difference. The authors suggest that the biology of metastatic prostate cancer may, in fact, be different in African-Americans and whites.
Kaposi’s Sarcoma-Associated Herpesvirus in Israel
Jews in Israel have one of the highest rates of Kaposi’s sarcoma in the developed world, but little is known about how the herpesvirus—KSHV—that causes this disease is transmitted in Middle Eastern and Mediterranean countries. Davidovici et al. (p. 194) identified a cohort of blood donors infected with hepatitis B virus (HBV) and followed them for 20 years, at which time they collected new sera from both members of the original cohort and their family members. All sera were tested for anti-KSHV antibodies. The authors found that birthplace (North African predicting highest risk) and spouse’s KSHV status were the best predictors of KSHV infection in married people; for children, the mother’s KSHV serostatus was most important. They also estimated that the seroprevalence of KSHV infection among Jews in Israel is 9.9%. Because the prevalence is higher in HBV chronic carriers, they concluded that HBV and KSHV were transmitted along similar pathways.
Helicobacter pylori and Gastric Cancer Risk
Persistent exposure to Helicobacter pylori without gastric epithelial cell invasion (carriage) is a risk factor for noncardia gastric cancer. Limburg et al. (p. 226) explored the subsite-specific gastric cancer risks associated with H. pylori seropositivity (a marker for persistent exposure) in Linxian, China. They found that seropositivity rates were statistically significantly higher for subjects with gastric cardia cancer and subjects with noncardia gastric cancer than for cancer-free control subjects. They conclude that H. pylori carriage may increase the risk of cancer throughout the stomach.
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