© 1999 by Oxford University Press
Journal of the National Cancer Institute, Vol. 91, No. 6, 487,
March 17, 1999
© 1999 Oxford University Press
IN THIS ISSUE |
Tumor shrinkage is a common end point used in screening new cytotoxic agents. The standard criterion for partial response is a decrease of 50% or more in the sum of individual products of two tumor measurements: the maximum diameter of a lesion and the largest diameter perpendicular to it. Theoretically, the simple sum of the maximum diameters of individual tumors is more linearly related to cell kill than is the sum of the bidimensional products. James et al. (p. 523) hypothesized that a 30% decrease in the sum of the maximum diameters of all lesions may be sufficient to determine response, assuming tumors of spherical shape. Agreement between unidimensional and bidimen-sional measurements was very high (kappa statistic for concordance for overall response, 0.95). The investigators conclude that unidimensional measurement (of the maximum diameter) is sufficient to assess tumor response when screening potential new drugs.
Energy Intake and Prostate Cancer
A sedentary lifestyle coupled with overeating is thought to be associated with an increased incidence of prostate cancer. Mukherjee et al. (p. 512) investigated the effects of energy intake on prostate tumor growth and biomarkers in experimental animals, using two transplantable, androgen-sensitive prostate tumor models: the Dunning R3327-H adenocarcinoma in rats and the LNCaP human prostate carcinoma in severe combined immunodeficient mice. R3327-H tumors were smaller in energy-restricted or castrate (androgen-deprived) rats than in control rats fed ad libitum. Energy-restricted rats exhibited changed tumor architecture that was characterized by increased stroma and more homogeneous and smaller glands. Thirty percent reduction in the intake of carbohydrate, lipid, or total diet produced similar inhibition of growth of R3327-H and LNCaP tumors. The evaluation of different tumor markers in both models indicated that energy restriction reduces prostate tumor growth by inhibiting the development of tumor blood vessels.
In an accompanying editorial, Bosland, Oakley-Girvan, and Whittemore (p. 489) say that Mukherjee et al. describe the first carefully designed experiments addressing the relationship between fat intake and energy intake and prostate cancer. Because of uncertainties in extrapolating results from rodents to humans and because of a lack of understanding of the mechanisms that underlie the observed relationships between diet and prostate cancer, the editorial writers question the direct application of these findings to people.
Dietary Fat Intake and Breast Cancer
Dietary fat has been the major focus in the search for dietary causes of breast cancer, but its importance remains controversial. On the other hand, compelling evidence exists implicating estrogens as a risk factor in this disease. Wu et al. (p. 529) conducted a meta-analysis of 13 dietary fat intervention studies, testing for an association between reduced fat intake and lower serum estradiol levels, and reviewed the nature of the evidence provided by prospective analytic studies of fat consumption and breast cancer risk. Consistent with reduced intake of fat, statistically significant reductions were found in serum estradiol levels in premenopausal and postmenopausal women combined (-13.4%) and separately (premenopausal, -7.4%, and postmenopausal, -23.0%). These results suggest that dietary fat reduction can lower serum estradiol levels and thereby lessen the risk of developing breast cancer, the investigators say.
In an editorial, Ballard-Barbash et al. (p. 492) conclude that the meta-analysis by Wu et al. represents a first effort in the attempt to quantify the potential effect of reducing dietary fat on serum estradiol levels. They note that strong correlations between diverse dietary components, many of which may have similar effects on serum estradiol, limit our ability to identify an independent effect of a single dietary factor. The editorialists make several recommendations for the conduct of future studies and meta-analyses on this issue.
Cervical Cancer: Is HPV Necessary?
Almost invariably, researchers who test cervical cancer specimens for DNA from human papillomavirus (HPV) find the sequences present. But can we conclude that HPV is a necessary cause of the cancer? In a commentary, Franco et al. (p. 506) investigate the effect of misclassification of exposure to HPV on researchers' ability to differentiate between necessary and nonnecessary causes of cervical cancer. By use of computer models, Franco et al. estimated relative risks of cervical intraepithelial neoplasia, a precursor of invasive cervical cancer, for different levels of misclassification of infection and of cumulative risks of cervical cancer given exposure or nonexposure to HPV. The authors conclude from their model that, at even relatively modest levels of misclassification of exposure, the ability of traditional epidemiology to distinguish necessary causes is completely lost.
Cigarette Smoking, Nutritional Status, and Pancreatic Cancer
Age and cigarette smoking are associated with greater risk for pancreatic cancer, while a protective role is played by consumption of fruits and vegetables. The latter represent major dietary sources of folates, suggesting a role for factors influencing cellular methylation reactions. To address the interplay of these risk and protective factors, Stolzenberg-Solomon et al. (p. 535) conducted a nested case-control study within the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study cohort of male Finnish smokers aged 50-69 years. The authors examined folate, pyridoxal-5'-phosphate, and other methyl-group indicators in the serum of 126 case subjects and 247 control subjects. Their results support the hypothesis that maintaining adequate folate and pyridoxine status reduces the risk of pancreatic cancer in older male smokers and confirm the risk associated with smoking.
Diabetes and Colorectal Cancer
Non-insulin-dependent diabetes mellitus (type 2) and colon cancer share several risk factors (i.e., obesity, physical inactivity, and higher intake of refined carbohydrates). In a prospective study, Hu et al. (p. 542) examined the possibility of a relationship between diabetes and the risk of colorectal cancer in a cohort of 118,403 women aged 30 through 55 years enrolled in the Nurses' Health Study. These women were without previously diagnosed cancer at baseline in 1976. The findings of Hu et al. support the hypothesis that type 2 diabetes is associated with an increased risk of colon cancer in women.
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