Biomedical subjects
E Sterns
Publications and source records attributed to E Sterns.
Mammographic density in women on postmenopausal hormone replacement therapy.
BACKGROUND: Studies have suggested that mammographic density and pattern are affected by hormone replacement therapy (HRT) and may influence breast diagnosis. Because 40% of breast cancers diagnosed at our center are mammographically detected while still clinically occult, mammographic sensitivity is crucial. For this reason we studied the effect of HRT on mammographic density. METHODS: During a period of 18 months we studied consecutive women older than 54 years attending for breast screening. We recorded HRT use and dosing regimes. A breast density score (BDS) was developed and applied to all mammograms. RESULTS: Mammograms of 148 HRT users were compared with those of 158 nonusers. HRT users had a significantly higher mean density score (4.7 versus 3.4; p < 0.001). Only 11% of non-HRT users had high scores compared with 37% among HRT users (p < 0.001). The significant difference remained when women were stratified by age. Duration of HRT (longer or shorter than 5 years) did not affect density scores. CONCLUSIONS: HRT is associated with a significant increase in breast density. In turn, density and mammographic sensitivity are related. The possibility that increased breast density will hamper mammographic diagnosis of clinically occult cancers is worrisome.
Localization of platelet-derived growth factor beta receptor expression in the periepithelial stroma of human breast carcinoma.
Platelet-derived growth factor (PDGF) BB is secreted by most human breast carcinoma cells; however, only recently have PDGF beta receptors been demonstrated in malignant breast tissue. In the present study, the tissue localization of PDGF beta receptor expression was studied in human breast carcinoma and nonmalignant breast tissues stained using both immunofluorescence and immunoperoxidase techniques. We examined a total of 29 cases of breast carcinomas, which showed both in situ and invasive components. PDGF beta receptor staining was localized in the periepithelial stroma and was particularly intense in regions immediately adjacent to carcinoma in situ components in all tumors examined. A diffuse low level of PDGF beta receptor staining was seen throughout the stroma of eight nonmalignant breast tissues as well as of nonmalignant regions of tumor tissues. Image analysis was used to assess the coincidence of staining of PDGF beta receptor with epithelial or stromal cells in 13 of the 29 tumor tissues studied. Less than 5% of malignant ductal epithelium or myoepithelium showed PDGF beta receptor staining. Analysis with stromal cell type-specific markers indicated significant localization of PDGF beta receptor primarily within alpha smooth muscle actin-staining cells (32%) and vascular endothelial cells (41%) in the periepithelial stroma. PDGF beta receptor positivity was strongly associated with periepithelial stromal cells adjacent to the basement membrane surrounding regions of carcinoma in situ but was less intense in regions of invasive carcinoma where basement membrane was degraded. The absence of PDGF beta receptors on carcinoma cells and their presence in the surrounding stroma suggest a paracrine stimulation of adjacent stromal tissue by malignant epithelial cells in human breast tumors.
Natural killer cell activity in women at "high risk" for breast cancer, with and without benign breast syndrome.
This study is an analysis of natural killer cell (NK) function in 155 women repeatedly tested over a 5-year period while attending breast screening clinics because of one or more of the following risk factors: family history-breast cancer in a close female relative (relative risk = 1.2-9); personal history-early menarche, non-parity, late menopause, etc. (relative risk = 1.3-3); clinical benign breast syndrome-localized and diffuse (relative risk = 2-4). Contrary to expectations, the high-risk group as a whole had significantly higher than normal relative NK function vs K562 (1.21 +/- 0.06 vs 1.00 +/- 0.06) (p less than 0.02). Division into subgroups showed that the NK activities in patients with positive family histories, personal histories, or both, were exactly the same as normal values and that the increased NK function in the high-risk group as a whole was due to those donors with benign breast syndrome (BBS). This group was also subdivided and the results were compared with the high-risk patients with no BBS. The NK activity of the group having diffuse BBS (1.67 +/- 0.05, n = 32) was significantly higher than that of the "No BBS" group (1.07 +/- 0.07, n = 102) (p less than 0.025). A paired "t'-test performed on data from 7 patients who had no BBS and diffuse BBS at different times showed a significant difference of p less than 0.001, suggesting that the elevated NK activity is a reaction to the hormonal factors which cause this condition.