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Most epithelial hyperplasias of the human breast indicate an increased likelihood of carcinoma development, and the majority are best understood as markers or indicators of higher risk. Prospective studies of women with hyperplasia biopsied in the premammographic era indicate that about 70 per cent of women had mild or no hyperplastic epithelial alterations and experienced no increase in the risk of subsequent carcinoma. About 25 per cent of women had well-developed hyperplastic changes associated with a risk 1.5 to 2.0 times that of the general population controlled for age and length of follow-up. Somewhat fewer than 5 per cent of women had specific patterns of atypical hyperplasia that approached the patterns of carcinoma in situ. The women with atypical hyperplasia had a risk of cancer four to five times that of the general population, or about half the risk associated with microscopic carcinoma in situ. Only ductal carcinoma in situ should be considered without question to be an intrinsically precancerous lesion because of its regular association with recurrence at the site of its initial diagnosis. No follow-up studies of comparable type involving women with mammographically detected lesions are as yet available. However, it is clear that the incidence of atypical hyperplasia is higher in mammographically directed biopsies. The principal therapeutic implication of these premalignant lesions is a need for intensified breast cancer surveillance and screening for these patients.
Epithelial hyperplasia of the breast carries an increased likelihood of carcinoma development, with most lesions best understood as markers of higher risk. The indication of increased cancer risk for more worrisome or complex histologic patterns has been supported in many studies. About 25% of women who underwent biopsies in the premammographic era had well-developed hyperplastic changes associated with an elevated risk of 1.5 to 2.0 times that of the general population when age and length of time of follow-up were considered. Somewhat fewer than 5% of women had specific patterns of atypical hyperplasia (AH) that approached the criteria of carcinoma in situ (CIS). These women with AH had a risk of cancer four to five times that of the general population, or about one half the risk associated with microscopic CIS. Only ductal CIS should be considered without question to be an intrinsic precancerous lesion because of its regular association with recurrence at the site of its initial diagnosis. Further studies indicated an appreciable interaction between AH and other nonanatomic risk factors, particularly a family history of breast cancer. Also, lower dosage estrogen replacement after menopause does not affect risk in any histologically defined group. The atypical hyperplastic lesions are more common in women undergoing biopsies on the indication of mammographic calcifications than because of palpable masses. The primary therapeutic implications of these premalignant lesions are intensified breast cancer surveillance and screening for these patients.
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 women, 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 of 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 about 10). 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 histology.(ABSTRACT TRUNCATED AT 250 WORDS)