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ABSTRACT: Experimental evidence provides strong support for anti-carcinogenic effects of calcium and vitamin D with respect to breast cancer. Observational epidemiologic data also provide some support for inverse associations with risk. We tested the effect of calcium plus vitamin D supplementation on risk of benign proliferative breast disease, a condition which is associated with increased risk of breast cancer. We used the Women's Health Initiative randomized controlled trial. The 36,282 participants were randomized either to 500 mg of elemental calcium as calcium carbonate plus 200 IU of vitamin D(3) (GlaxoSmithKline) twice daily (n = 18,176) or to placebo (n = 18,106). Regular mammograms and clinical breast exams were performed. We identified women who had had a biopsy for benign breast disease and subjected histologic sections from the biopsies to standardized review. After an average follow-up period of 6.8 years, 915 incident cases of benign proliferative breast disease had been ascertained, with 450 in the intervention group and 465 in the placebo group. Calcium plus vitamin D supplementation was not associated with altered risk of benign proliferative breast disease overall (hazard ratio = 0.99, 95% confidence interval = 0.86-1.13), or by histologic subtype. Risk varied significantly by levels of age at baseline, but not by levels of other variables. Daily use of 1,000 mg of elemental calcium as calcium carbonate plus 400 IU of vitamin D(3) for almost 7 years by postmenopausal women did not alter the overall risk of benign proliferative breast disease.
Breast Cancer Research and Treatment 11/2008; 116(2):339-50. · 4.43 Impact Factor
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ABSTRACT: Menstrual and reproductive history and postmenopausal hormone use are well-established risk factors for breast cancer. However, previous studies that have assessed these factors in association with risk of benign proliferative epithelial disorders (BPED) of the breast, putative precursors of breast cancer, have yielded inconsistent findings. To investigate these associations, we conducted a cohort study among 68,132 postmenopausal women enrolled in the Women's Health Initiative randomized clinical trials. Women were prospectively followed and those reporting an open surgical biopsy or a core needle biopsy had histological sections obtained for centralized pathology review. Over an average of 7.8 years of follow-up, we identified 1,792 women with BPED of the breast. We used Cox proportional hazards models to estimate hazard ratios (HRs) and 95% confidence limits (CLs) for the associations of interest. Menstrual and reproductive histories were not associated with risk of BPED of the breast, overall or by histological subtype. Women who had used postmenopausal hormones for 15 years or more had a two-fold increase in risk of BPED of the breast compared to women who had never used postmenopausal hormones (HR = 2.03 95% CL = 1.73, 2.38) and the increase in risk was observed for both BPED of the breast without atypia and for atypical hyperplasia. Furthermore, the risk of BPED of the breast decreased with time since cessation of use so that there was essentially no increase in risk 5 or more years after ending use (HR for stopping >or=5 years earlier = 0.96, 95%CL = 0.79, 1.16; HR for stopping <5 years earlier = 1.32, 95% CL = 1.08,1.61).
Breast Cancer Research and Treatment 04/2008; 114(1):113-20. · 4.43 Impact Factor
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Jules J Berman,
Jorge Albores-Saavedra,
David Bostwick,
Ronald Delellis,
John Eble,
Stanley R Hamilton,
Ralph H Hruban,
George L Mutter, David Page,
Thomas Rohan,
William Travis,
Donald E Henson
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ABSTRACT: Precancers are lesions that precede the appearance of invasive cancers. The successful prevention or treatment of precancers has the potential to eliminate deaths due to cancer.
A National Cancer Institute-sponsored Conference on Precancer was convened on November 8-9, 2004, at The George Washington University Medical Center, Washington, DC. A definition of precancers was developed over 2 days of Conference discussions.
The following five criteria define a precancer: (1) evidence must exist that the precancer is associated with an increased risk of cancer; (2) when a precancer progresses to cancer, the resulting cancer arises from cells within the precancer; (3) a precancer differs from the normal tissue from which it arises; (4) a precancer differs from the cancer into which it develops, although it has some, but not all, of the molecular and phenotypic properties that characterize the cancer; (5) there is a method by which the precancer can be diagnosed.
The Conference participants developed a general definition for precancers that would provide a consistent and clinically useful way of distinguishing precancers from all other types of lesions. It was recognized that many precancerous lesions may not meet this strict definition, but the group felt it was necessary to define criteria that will help standardize clinical and biological studies. Furthermore, a set of defining criteria for putative precancer lesions will permit pathologists to build a diagnostically useful taxonomy of precancers based on specified clinical and biological properties. Precancers thus characterized can be classified into clinically relevant sub-groups based on shared properties (i.e. biomarkers, oncogenes, common metabolic pathways, responses to therapy, etc.). Publications that introduce newly described precancer entities should describe how each of the five defining criteria apply. This manuscript reviews the proposed definition of precancers and suggests how pathologists, oncologists and cancer researchers may determine when these criteria are satisfied.
Cancer Detection and Prevention 02/2006; 30(5):387-94. · 2.52 Impact Factor
