Effects of Estrogen and Estrogen–Progestin on Mammographic Parenchymal Density

Greendale, Gail A.; Reboussin, Beth A.; A, Sie; Singh, Heena; Olson, Linda K.; Gatewood, Olga M. B.; Bassett, Lawrence W.; Wasilauskas, Carol H.; Bush, Trudy L.; Barrett-Connor, E.

doi:10.7326/0003-4819-130-4_part_1-199902160-00003

Cited by 361 publications

(138 citation statements)

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“…Recent epidemiological studies have shown that postmenopausal hormone replacement therapy in the form of estrogen -progestin replacement therapy (EPRT) increases breast cancer risk to a much greater extent than estrogen (alone) replacement therapy (ERT; Magnusson et al, 1999;Ross et al, 2000;Schairer et al, 2000). These results are supported by the finding that mammographic densities are increased much more by EPRT than ERT (Greendale et al, 1999), and so is breast-cell proliferation (Hofseth et al, 1999).In the present study, we evaluated differences in ovarian function in African-American, Latina and non-Latina White young women in Los Angeles who were recruited as part of a crosssectional investigation of the frequency of anovulation and of circulating serum E 2 and P 4 levels among 'normally cycling' nulliparous women. …”

supporting

confidence: 80%

Ethnic differences in ovulatory function in nulliparous women

et al. 2002

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African-American women have a long-standing approximately 20% higher breast cancer incidence rate than USA White women under age 40 while rates among Latinas are lower than those of Whites. The reasons for this are not clear, however they may be due to ethnic differences in circulating oestradiol and progesterone levels. In a cross-sectional study, we investigated whether anovulation frequency and circulating serum oestradiol and/or progesterone levels vary among normally cycling nulliparous African-American (n=60), Latina (n=112) and non-Latina White (n=69) women. Blood and urine specimens were collected over two menstrual cycles among healthy 17-to 34-year-old women. Frequency of anovulation was greater among White women (nine out of 63, 14.3%) than African-American women (four out of 56, 7.1%) or Latina women (seven out of 102, 6.9%), although these differences were not statistically significant. African-American women had 9.9% (P=0.26) higher follicular phase oestradiol concentrations than Latina women and 17.4% (P=0.13) higher levels than White women. African-American women also had considerably higher levels of luteal phase oestradiol (vs Latinas, +9.4%, P=0.14; vs Whites, +25.3%, P=0.003) and progesterone (vs Latinas, +15.4%, P=0.07; vs Whites, +36.4%, P=0.002). Latina women were also observed to have higher follicular oestradiol, and luteal oestradiol and progesterone levels than White women (follicular oestradiol: +6.8%, P=0.48; luteal oestradiol: +14.6%, P=0.04; luteal progesterone: +18.2%, P=0.06). These results suggest that exposure to endogenous steroid hormones may be greater for young African-American and Latina women than for Whites. British Journal of Cancer (2002) (Gray et al, 1980;Parkin et al, 1997;SEER Program, 2001). The reasons for this are not clear, however they may be due to ethnic differences in circulating oestradiol (E 2 ) and progesterone (P 4 ) levels. Oestradiol is an established breast-cell mitogen, and considerable epidemiological and experimental evidence indicates that women with higher circulating levels are at greater risk of developing breast cancer (Bernstein and Ross, 1993; Pike et al, 1993;Thomas et al, 1997;Hankinson et al, 1998). Considerable evidence also exists indicating that progestins play an important role in breast carcinogenesis. Recent epidemiological studies have shown that postmenopausal hormone replacement therapy in the form of estrogen -progestin replacement therapy (EPRT) increases breast cancer risk to a much greater extent than estrogen (alone) replacement therapy (ERT; Magnusson et al, 1999;Ross et al, 2000;Schairer et al, 2000). These results are supported by the finding that mammographic densities are increased much more by EPRT than ERT (Greendale et al, 1999), and so is breast-cell proliferation (Hofseth et al, 1999).In the present study, we evaluated differences in ovarian function in African-American, Latina and non-Latina White young women in Los Angeles who were recruited as part of a crosssectional investigation of the frequency of anovulatio...

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supporting

confidence: 80%

Ethnic differences in ovulatory function in nulliparous women

et al. 2002

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“…The increment was greater in response to EPT than to ET in the terminal ductal lobular unit. Greendale et al 20 , 21 and others 13 have shown that HT and particularly EPT increase mammographic density substantially over that with use of placebo or no therapy. However, no studies have correlated breast density and histologic changes in women using HT.…”

mentioning

confidence: 99%

Histologic changes in the breast with menopausal hormone therapy use

Harvey¹,

Santen²,

Petroni

et al. 2008

Menopause

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Objective-This retrospective study systematically compared mammographic density with histology in women receiving or not receiving menopausal hormone therapy (HT).Design-This study was approved by the institutional review board. Twenty-eight postmenopausal women using HT were matched with 28 postmenopausal women not using HT at the time of breast cancer diagnosis. Noncancerous tissue from mastectomy specimens was examined histologically to quantitate the content of fibrous stroma, ducts, and lobule types 1, 2, and 3. Tissue samples were also evaluated for estrogen receptor, progesterone receptor, and Ki67 activity in the ducts and lobules. Breast density was quantified by digitizing the contralateral mammogram and computer-assisted interactive thresholding.Results-High breast density in women using HT was correlated with greater fibrous stroma (P = 0.020) and lobule type 1 (P = 0.016). Breast density also correlated with Ki67 activity in the ducts (P = 0.031) and lobules (P = 0.023) for both groups combined. Estrogen and progesterone receptors did not correlate with either breast density or HT use.Conclusions-Increased fibrous stroma and lobule type 1 are associated with increasing mammographic density in women using HT, independent of estrogen and progesterone receptor up-regulation. These findings suggest that increased breast density may be mediated through a paracrine effect. The increase in breast cancer risk with HT use may be due to an increase in target lobule type 1 cells.

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“…[34][35][36][37] In the PEPI trial, women in the 3 estrogen plus progestin groups had much greater increases in mammographic density (a predictor of breast cancer) than women in the estrogen or placebo groups. 38 In WHI, the HR for estrogen plus progestin was not higher in women with a family history or other risk factors for breast cancer, except for reported prior use of postmenopausal hormones. This may suggest a cumulative effect of years of exposure to postmenopausal hormones.…”

Section: Cancermentioning

confidence: 87%

Exercise and Risk of Breast Cancer

2003

JAMA

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Effects of Estrogen and Estrogen–Progestin on Mammographic Parenchymal Density

Abstract: Further study of the magnitude and meaning of increased mammographic density due to use of estrogen and estrogen-progestins is warranted because mammographic density may be a marker for risk for breast cancer.

Cited by 361 publications

References 34 publications

Ethnic differences in ovulatory function in nulliparous women

Ethnic differences in ovulatory function in nulliparous women

Histologic changes in the breast with menopausal hormone therapy use

Exercise and Risk of Breast Cancer

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