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  • 1
    Electronic Resource
    Electronic Resource
    Epidemiological approaches to primary and secondary prevention of cancer (1991)
    Springer
    Journal of cancer research and clinical oncology 117 (1991), S. 177-185 
    Details
    ISSN: 1432-1335
    Keywords: Cancer control ; Breast cancer ; Colorectal cancer ; Primary prevention ; Screening
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Primary prevention of cancer requires control of both involuntary and voluntary exposures. Involuntary exposures include carcinogens in air and water, and various forms of radiation. Often these exposures are difficult to characterise individually and difficult to study epidemiologically. Although it is unlikely that they account for more than a small proportion of cancers, it is important that we refine our techniques of study to facilitate their control. Voluntary (lifestyle) exposures are responsible for the majority of cancers. In many developed countries, tobacco accounts for approximately 30% of cancer deaths, and major public health endeavours are justified to reduce this toll. Dietary factors may be as important, with dietary fat the most important risk factor, vegetables and fruits being protective. In several studies, including a cohort study in Canada, dietary fat increases breast cancer risk, though other studies have been negative. The evidence for fat increasing the risk of colorectal is more consistent. Epidemiology has shown that secondary prevention of cancer is applicable by screening for breast cancer with mammography with or without physical examination in women age 50–69, and screening for cervix cancer in women age 25–60 with cervical cytology. Organised screening programmes are essential to ensure that a high proportion of women are screened, and that the tests are high quality with adequate quality control. Under these circumstances screening every 2 years for breast cancer and every 3 years for cervix cancer is cost-effective. Screening for other cancers cannot be recommended currently. There is a time to effect that must be recognised in planning primary or secondary prevention. Full effect of most primary activities will not be achieved for decades, screening may require a decade. Available knowledge must be applied now, however, to ensure the effect will eventually be seen, as is now occurring in some countries with the downturn in lung cancer mortality following smoking reduction in men.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01625422
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Non-dietary factors as risk factors for breast cancer, and as effect modifiers of the association of fat intake and risk of breast cancer (1997)
    Springer
    Cancer causes & control 8 (1997), S. 49-56 
    Details
    ISSN: 1573-7225
    Keywords: Breast cancer ; diet ; reproductive factors ; women
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract To assess more precisely the relative risks associated with established risk factors for breast cancer, and whether the association between dietary fat and breast cancer risk varies according to levels of these risk factors, we pooled primary data from six prospective studies in North America and Western Europe in which individual estimates of dietary fat intake had been obtained by validated food-frequency questionnaires. Based on information from 322,647 women among whom 4,827 cases occurred during follow-up: the multivariate-adjusted risk of late menarche (age15 years or more compared with under 12) was 0.72 (95 percent confidence interval [CI]=0.62-0.82); of being postmenopausal was 0.82 (CI=0.69-0.97); of high parity (three or more births compared with none) was 0.72 (CI=0.61-0.86); of late age at first birth (over 30 years of age compared with 20 or under) was 1.46 (CI=1.22-1.75); of benign breast disease was 1.53 (CI=1.41-1.65); of maternal history of breast cancer was 1.38 (CI=1.14-1.67); and history of a sister with breast cancer was 1.47 (CI=1.27-1.70). Greater duration of schooling (more than high-school graduation compared with less than high-school graduation) was associated significantly with higher risk in age-adjusted analyses, but was attenuated after controlling for other risk factors. Total fat intake (adjusted for energy consumption) was not associated significantly with breast cancer risk in any strata of these non-dietary risk factors. We observed a marginally significant interaction between total fat intake and risk of breast cancer according to history of benign breast disease, with fat intake being associated nonsignificantly positively with risk among women with a previous history of benign breast disease; no other significant interactions were observed. Risks for reproductive factors were similar to those observed in case-control studies; relative risks for family history of breast cancer were lower. We found no clear evidence in any subgroups of a major relation between total energy-adjusted fat intake and breast cancer.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1018431104786
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  • 3
    Electronic Resource
    Electronic Resource
    A case-cohort study of diet and risk of benign proliferative epithelial disorders of the breast (Canada) (1998)
    Springer
    Cancer causes & control 9 (1998), S. 19-27 
    Details
    ISSN: 1573-7225
    Keywords: Canada ; diet ; benign breast disease ; breast cancer ; women
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract A case-cohort analysis of the association between diet and risk of benign proliferative epithelial disorders (BPED) of the breast was undertaken within a cohort of 56,537 women who were enrolled in the Canadian National Breast Screening Study (NBSS) and who completed a self-administered dietary questionnaire. (The NBSS is a randomized controlled trial of screening for breast cancer in women aged 40 to 59 years.) BPED are thought to have premalignant potential. Specific hypotheses were that risk of BPED would increase with increasing energy-adjusted fat intake and decrease with increasing energy-adjusted vitamin A and fiber intake. Additionally, we explored the association between calcium intake and risk of BPED. During the active follow-up phase of the NBSS, 657 women in the dietary cohort were diagnosed with biopsy-confirmed incident BPED. For comparative purposes, a subcohort consisting of a random sample of 5,581 women was selected from the full dietary cohort. After exclusions for various reasons, the analyses were based on 545 cases and 4,921 non-cases. Overall, the results were almost uniformly null, and provided little support for the study hypotheses. Rate ratios (95 percent confidence intervals [CI]) for the highest cf the lowest quintile levels for total fat, retinol, β-carotene, fiber, and calcium were 0.88 (CI = 0.65-1.20), 0.97 (CI = 0.71-1.31), 0.94 (CI = 0.70-1.27), 1.11 (CI = 0.82-1.50), and 0.81 (CI = 0.60-1.07), respectively. There were too few cases of atypical BPED for meaningful analysis, but results for those whose BPED showed no atypia were similar to the overall results. Further analyses conducted separately in the screened and control arms of the NBSS also failed to provide strong support for dietary associations, as did those conducted separately for screen-detected and interval-detected BPED.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1008841118358
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    Paper (German National Licenses)
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