Publications

The relation between dietary vitamin A and the risk of invasive cervical cancer was evaluated using data from a hospital-based case-control study of 191 women with cervical cancer and 191 age-matched controls. There was no association between dietary retinoids and cervical cancer risk. Intake of dietary beta-carotene, on the other hand, was inversely and strongly related to the risk of cervical cancer. Compared to risks for women reporting a monthly intake of 150,000 or more international units (IU) of beta-carotene, the estimated relative risks for those with 100,000 to 149,000 and those with less than 100,000 IU per month were 2.8 and 6.1 respectively. The inverse association was not explained by any of the major identified risk factors for cervical cancer (including indicators of socio-economic status or sexual habits), or by differences in general characteristics and other lifestyle habits between cases and controls. Thus, although the uncertainties of the vitamin A measurements used are substantial, these findings support the hypothesis that dietary beta-carotene-or some related aspect of a vegetable-rich diet-is protective against invasive cervical cancer.

Dietary fats are thought to be important in the etiology of colon cancer. However, the evidence linking them is inconclusive. Studies on dietary protein, cholesterol and carbohydrate and the risk of colon cancer are also inconsistent. This study examined the association between dietary intake of protein, fats, cholesterol and carbohydrates, and the risk of colon cancer. Mailed questionnaires were completed by 1731 individuals with histologically confirmed cases of colon cancer and 3097 population controls between 1994 and 1997 in seven Canadian provinces. Measurements included socio-economic status, lifestyle habits and diet. A 69-item food frequency questionnaire was used to provide data on eating habits from two years before the study. Odds ratios (OR) and 95% confidence intervals (CI) were computed using unconditional logistic regression. The nutrients were categorized by quartiles based on the distributions among the controls. Intake of polyunsaturated fat, trans-fat and cholesterol were significantly associated with the risk of colon cancer; the ORs for the highest quartiles were 1.36 (95% CI, 1.02-1.80), 1.37 (95% CI, 1.10-1.71) and 1.42 (95% CI, 1.10-1.84), respectively. The association was stronger with proximal colon cancer (PCC). An increased risk was also observed with increasing intake of sucrose for both proximal and distal colon cancers; the ORs for the highest quartiles were 1.67 (95% CI, 1.22-2.29) for PCC and 1.58 (95% CI, 1.18-2.10) for distal colon cancer (DCC). An elevated risk of PCC was also found with increased lactose intake. Our findings provide evidence that a diet low in fat and sucrose could reduce the risk of various colon cancers.

A number of co-aggregations of cancers at different sites has been reported, including recognized syndromes (e.g., Li-Fraumeni), and aggregations between cancers at breast, stomach and ovary, between cancers at prostate, urinary tract and other sites, as well as between several tobacco-related neoplasms. In a network of case-control studies from Italy and Switzerland, including more than 12,000 cases of 13 different cancers, after controlling for multiple testing, significant associations emerged between oral and pharyngeal cancer and family history of laryngeal cancer (relative risk (RR): 3.3); esophageal cancer and family history of oral and pharyngeal cancer RR: 4.1; breast cancer and family history of colorectal cancer (RR: 1.5) and of hemolymphopoietic cancers (RR: 1.7); ovarian cancer and family history of breast cancer (RR: 2.3); and prostate cancer and family history of bladder cancer (RR: 3.4). Shared exposures to environmental factors within families account for some of the observed aggregations, together with heritable, and hence, genetic factors.

A positive association between the use of oral contraceptives and the risk of cervical neoplasia has been suggested by different sources. This paper examines epidemiologic evidence on this issue through pooled computation of relative risks emerging from 21 studies, subdivided into three main categories: studies based on routine cytologic screening programs, case-control investigations and prospective studies. The pooled estimates of the relative risks for ever vs never use of oral contraceptives were broadly similar and slightly above unity (1.4 from cytologic screening programs, 1.1 from case-control and 1.4 from prospective studies). The risk increased with duration of use and, generally, lower relative risk estimates derived from the older studies, necessarily based on short-term use of oral contraceptives. A particularly limited increase in risk was apparent from case-control investigations. Furthermore, when allowance was made for the major covariates (mostly indicators of sexual habits), a noticeable decrease in the excess risk was evident. In conclusion, although statistical significance of moderate differences in risk can be obtained by pooling data from several studies, a risk of the magnitude of that for the association between oral contraceptives and cervical neoplasia may well be due to bias and confounding. In addition, since sexual behavior only indicates the probability of having been exposed to some sexually transmitted agent (most likely human papilloma virus), the greatest additional contribution may come from a case-control study in which adjustment for such exposure is possible.

Between November 1981 and March 1983, data were collected to evaluate risk factors for benign breast lesions in a case-control study based on 288 women with histologically proven benign breast disease, admitted for biopsy to the Tumor Institute of Milan, and 285 age-matched controls. Questions were asked about menstrual and reproductive characteristics, marital status, education, history of various diseases, and lifetime use of oral contraceptives and other hormonal treatments. Nulliparity or low parity, late age at first birth, and late menopause were associated with an increased risk of benign breast disease. The elevated risk associated with late age at first birth was not accounted for by parity. Early age at menarche was associated with an increased risk, but the estimate was not statistically significant. The data do not suggest that the use of oral contraceptives or other female hormones (such as estrogen replacement therapy) is related to the risk of benign breast disease. Risk was apparently lower, however, among current and long-term oral contraceptive users. There was no evidence of a trend with reference to body mass index. The present data indicate a substantial agreement between the risk factors for (pathologically confirmed) benign and malignant breast disease, not only directly, by showing a relationship with parity, age at first birth, and age at menopause, but also indirectly, by failing to produce evidence that greater weight or the use of oral contraceptives has a protective effect.