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Indicators of increased breast cancer risk in humans
Author(s) -
Page David L.,
Dupont William D.
Publication year - 1992
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.240501130
Subject(s) - breast cancer , family history , medicine , atypia , relative risk , menopause , absolute risk reduction , population , atypical hyperplasia , gynecology , cancer , obstetrics , risk factor , oncology , hyperplasia , pathology , confidence interval , environmental health
Specific atypical histological patterns of epithelial hyperplasia (AH) indicate a medically relevant risk of breast cancer development in 5‐10% of women with otherwise benign biopsies. This risk is about four times that of similar womer, i.e. , of the same age and at risk for the same length of time. These relative risks are not stable with time and fall 10‐15 years after detection. Absolute risk for invasive breast cancer after AH is about 10% in 10‐15 years after biopsy and is most certain for perimenopausal women. Proliferative disease without atypia predicts only a slight elevation of risk with a relative risk (RR) of 1.5 to 2 times that to the general population. There is such a strong interaction between family history and AH that it is relevant to consider women with atypical hyperplasia who have a positive family history (FH) of breast cancer separately from those who do not. The absolute risk of breast cancer development in women with AH without a FH was 8% in 10 years (RR about 4), whereas those with a positive family history experienced a risk of about 20% at 15 years (RR of about10). This interaction of AH and FH has also been observed in other recent studies. Low replacement doses of conjugated estrogen after menopause do not further elevate risk beyond that identified by hostology. In our cohort of over 10,000 women who underwent benign breast biopsy in Nashville, TN, we found no association between proliferative breast disease without atypia and a first‐degree FH of breast cancer; the prevalence of these lesions was 27% and 29% in women with and without such a history, respectively. Women with this family hostory did, however, have a higher prevalence of AH than did women without this history (4.8% versus 3.9%, respectively; p = 0.02). It would appear that these histologic lesions are not due to an estrogen effect, but are an unrelated phenomenon, and that FH of breast cancer is not related to the proliferative lesions associated with only slightly increased risk of breast cancer.

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