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Mammographic breast density and tolerance for short-term postmenopausal hormone therapy suspension.

ABSTRACT: Breast density tends to decrease when women stop taking hormone therapy (HT). Some women find HT cessation difficult to tolerate, possibly because of fluctuations in endogenous hormone levels and vasomotor symptoms. We hypothesized that women with dense breasts might have lower tolerance for short-term HT suspension than do women with fatty breasts.As part of the Radiologic Evaluation And breast Density (READ) trial, we randomly assigned 881 women aged 45-80 with a prior screening (index) mammogram to suspend HT for 1 or 2 months before their next screening (study) mammogram. We measured continuous breast density on index mammograms using computer-assisted thresholding. At study mammograms, women indicated tolerance for stopping HT from 1 (extremely difficult) to 7 (very easy). Using linear regression, we evaluated the association between index breast density and tolerance after cessation, adjusting for age, body mass index (BMI), HT type, randomization group, and vasomotor symptoms.A higher percentage of breast density was associated with lower unadjusted mean tolerance scores (tolerance 4.27, 95% confidence interval [CI] 3.77-4.77 for women with > or =50% density, and 4.73, 95% CI 4.45-5.01 for women with <10% density, not a statistically significant difference). In adjusted analyses, neither percent breast density nor dense breast area was associated with tolerance for HT suspension.Although HT use affects breast density, tolerance for suspending HT is not associated with breast density. Women with dense breasts have the greatest potential for decreases in density after HT cessation; they should tolerate stopping HT as well as women with fatty breasts.

SUBMITTER: Aiello Bowles EJ

PROVIDER: S-EPMC2941404 | biostudies-literature | 2010 Aug

REPOSITORIES: biostudies-literature

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Mammographic breast density and tolerance for short-term postmenopausal hormone therapy suspension.

Aiello Bowles Erin J EJ Anderson Melissa L ML Reed Susan D SD Newton Katherine M KM Fitzgibbons E Dawn ED Seger Deborah D Buist Diana S M DS

Journal of women's health (2002) 20100801 8

<h4>Background</h4>Breast density tends to decrease when women stop taking hormone therapy (HT). Some women find HT cessation difficult to tolerate, possibly because of fluctuations in endogenous hormone levels and vasomotor symptoms. We hypothesized that women with dense breasts might have lower tolerance for short-term HT suspension than do women with fatty breasts.<h4>Methods</h4>As part of the Radiologic Evaluation And breast Density (READ) trial, we randomly assigned 881 women aged 45-80 wi ...[more]

PMID: 20575711

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Project description:BackgroundWithout population-based evidence, some clinicians recommend short-term suspension of hormone therapy to improve the performance of mammography. Hormone therapy increases breast density, and abnormal screening mammograms are more common among women with denser breasts and among women using hormone therapy.ObjectiveTo test whether 1 to 2 months of hormone therapy suspension before screening mammography decreases additional mammographic imaging (recall) in women age 45 to 80 years.Design3-group randomized, controlled trial.SettingIntegrated health plan in western Washington from 2004 to 2007.Patients1704 women age 45 to 80 years who used hormone therapy at their most recent screening (index) mammography, were due for screening (study) mammography, and were still using hormone therapy.InterventionBlock random assignment (by breast density and hormone therapy type) to no hormone therapy suspension (n = 567) or suspension for 1 month (n = 570) or 2 months (n = 567) before study mammography. One blinded expert radiologist interpreted all mammograms.MeasurementsRecall was the primary outcome, and change in mammographic breast density (percentage and dense area) between the index and study mammograms was the secondary outcome.ResultsMammography recall rates were 11.3% (61 of 542 women in the no-suspension group), 12.3% (50 of 478 women in the 1-month suspension group), and 9.8% (44 of 451 women in the 2-month suspension group). No subgroups were identified in which brief suspension of hormone therapy resulted in decreased mammography recall. With suspension, decreases in percentage of breast density were orderly and statistically significant: 0.1% (no-suspension group), -0.9% (1-month suspension group), and -1.5% (2-month suspension group). Similar ordered decreases were observed for dense area. Women in the suspension groups experienced increased menopause symptoms.LimitationsResults can only be generalized to women age 45 to 80 years who have used hormone therapy for at least 1 year and will consider short-term suspension; most eligible women (61%) declined participation. Mammography recall was determined by 1 expert radiologist.ConclusionBrief hormone therapy suspension was associated with small changes in breast density and did not affect recall rates. No evidence supports short-term hormone therapy suspension before mammography.

Project description:INTRODUCTION:Mammographic density (MD) is one of the strongest known breast cancer risk factors. Estrogen and progestin therapy (EPT) has been associated with increases in MD. Dense breast tissue is characterized by increased stromal tissue and (to a lesser degree) increased numbers of breast epithelial cells. It is possible that genetic factors modify the association between EPT and MD, and that certain genetic variants are particularly important in determining MD in hormone users. We evaluated the association between MD and 340 tagging single nucleotide polymorphisms (SNPs) from about 30 candidate genes in hormone metabolism/growth factor pathways among women who participated in the Norwegian Breast Cancer Screening Program (NBCSP) in 2004. METHODS:We assessed MD on 2,036 postmenopausal women aged 50 to 69 years using a computer-assisted method (Madena, University of Southern California) in a cross-sectional study. We used linear regression to determine the association between each SNP and MD, adjusting for potential confounders. The postmenopausal women were stratified into HT users (EPT and estrogen-only) and non-users (never HT). RESULTS:For current EPT users, there was an association between a variant in the prolactin gene (PRL; rs10946545) and MD (dominant model, Bonferroni-adjusted P (Pb) = 0.0144). This association remained statistically significant among current users of norethisterone acetate (NETA)-based EPT, a regimen common in Nordic countries. Among current estrogen-only users (ET), there was an association between rs4670813 in the cytochrome P450 gene (CYP1B1) and MD (dominant model, Pb = 0.0396). In never HT users, rs769177 in the tumor necrosis factor (TNF) gene and rs1968752 in the region of the sulfotransferase gene (SULT1A1/SULT1A2), were significantly associated with MD (Pb = 0.0202; Pb = 0.0349). CONCLUSIONS:We found some evidence that variants in the PRL gene were associated with MD in current EPT and NETA users. In never HT users, variants in the TNF and SULT1A1/SULT1A2 genes were significantly associated with MD. These findings may suggest that several genes in the hormone metabolism and growth factor pathways are implicated in determining MD.

Project description:We examined the associations of mammographic breast density with breast cancer risk by tumor aggressiveness and by menopausal status and current postmenopausal hormone therapy.This study included 2596 invasive breast cancer cases and 4059 controls selected from participants of four nested case-control studies within four established cohorts: the Mayo Mammography Health Study, the Nurses' Health Study, Nurses' Health Study II, and San Francisco Mammography Registry. Percent breast density (PD), absolute dense (DA), and non-dense areas (NDA) were assessed from digitized film-screen mammograms using a computer-assisted threshold technique and standardized across studies. We used polytomous logistic regression to quantify the associations of breast density with breast cancer risk by tumor aggressiveness (defined as presence of at least two of the following tumor characteristics: size ?2 cm, grade 2/3, ER-negative status, or positive nodes), stratified by menopausal status and current hormone therapy.Overall, the positive association of PD and borderline inverse association of NDA with breast cancer risk was stronger in aggressive vs. non-aggressive tumors (?51 vs. 11-25% OR 2.50, 95% CI 1.94-3.22 vs. OR 2.03, 95% CI 1.70-2.43, p-heterogeneity = 0.03; NDA 4th vs. 2nd quartile OR 0.54, 95% CI 0.41-0.70 vs. OR 0.71, 95% CI 0.59-0.85, p-heterogeneity = 0.07). However, there were no differences in the association of DA with breast cancer by aggressive status. In the stratified analysis, there was also evidence of a stronger association of PD and NDA with aggressive tumors among postmenopausal women and, in particular, current estrogen+progesterone users (?51 vs. 11-25% OR 3.24, 95% CI 1.75-6.00 vs. OR 1.93, 95% CI 1.25-2.98, p-heterogeneity = 0.01; NDA 4th vs. 2nd quartile OR 0.43, 95% CI 0.21-0.85 vs. OR 0.56, 95% CI 0.35-0.89, p-heterogeneity = 0.01), even though the interaction was not significant.Our findings suggest that associations of mammographic density with breast cancer risk differ by tumor aggressiveness. While there was no strong evidence that these associations differed by menopausal status or hormone therapy, they did appear more prominent among current estrogen+progesterone users.

Project description:Mammographic breast density (MBD) is a risk factor for breast cancer, but its molecular basis is poorly understood. Growth factors stimulate cellular and epithelial proliferation and could influence MBD via these mechanisms. Studies investigating the associations of circulating growth factors with MBD have, however, yielded conflicting results especially in postmenopausal women. We, therefore, investigated the associations of plasma growth factor gene expression [insulin-like growth factor (IGF)-1, IGF-binding protein 3, FGF-1, FGF-12, TGFβ1 and bone morphogenetic protein (BMP)-2] with MBD in postmenopausal women. We used NanoString nCounter platform to quantify plasma growth factor gene expression and Volpara to evaluate volumetric MBD measures. We investigated the associations of growth factor gene expression with MBD using both multiple linear regression (fold change) and multinomial logistic regression models, adjusted for potential confounders. The mean age of the 368 women enrolled was 58 years (range, 50-64). In analyses using linear regression models, one unit increase in IGF-1 gene expression was associated with a 35% higher volumetric percent density (VPD, 1.35; 95% confidence interval (CI), 1.13-1.60; P = 0.001). There were suggestions that TGFβ1 gene expression was positively associated with VPD while BMP-2 gene expression was inversely associated with VPD, but these were not statistically significant. In analyses using multinomial logistic regression, TGFβ1 gene expression was 33% higher (OR = 1.33; 95% CI, 1.13-1.56; P = 0.0008) in women with extremely dense breasts than those with almost entirely fatty breasts. There were no associations between growth factor gene expression and dense volume or nondense volume. Our study provides insights into the associations of growth factors with MBD in postmenopausal women and requires confirmation in other study populations.Prevention relevanceMammographic breast density is a strong risk factor for breast cancer. Understanding its underlying biological mechanisms could have utility in breast cancer prevention.

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Mammographic breast density and tolerance for short-term postmenopausal hormone therapy suspension.

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Mammographic breast density and tolerance for short-term postmenopausal hormone therapy suspension.

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