Does Menopausal Hormone Replacement Therapy Interact With Known Factors to Increase Risk of Breast Cancer?

Ursin, Giske; Tseng, Chiu-Chen; Paganini‐Hill, Annlia; Enger, Shelley M.; Wan, Peggy; Formenti, Silvia; Pike, Malcolm C.; Ross, Ronald K.

doi:10.1200/jco.2002.20.3.699

Cited by 58 publications

(39 citation statements)

References 21 publications

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“…Several studies have suggested that EPRT is associated with greater increases in risk in leaner than heavier women [5,8], which is consistent with the collaborative reanalysis of the world's data [17]. Other studies have reported similar increases in risk in lean and heavy women [20,23]. Increases in risk have been noted for both testosterone-derived progestins [7,8] and progesterone-derived progestins [5,6],[18-20,22].…”

Section: Hormone Replacement Therapy and Breast Cancer Risksupporting

confidence: 73%

Progesterone receptors - animal models and cell signaling in breast cancer: Implications for breast cancer of inclusion of progestins in hormone replacement therapies

Schairer

2002

Breast Cancer Res

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244 CI = confidence interval; EPRT = estrogen-progestin replacement therapy; ERT = estrogen replacement therapy; HRT = hormone replacement therapy; RR = relative risk. Breast Cancer Research Vol 4 No 6 Schairer IntroductionMenopausal hormone replacement therapy (HRT), most commonly including estrogens alone or in combination with progestins, is used to alleviate menopausal symptoms and to prevent osteoporosis. Progestins are prescribed to offset the increased risk for endometrial cancer associated with estrogen replacement therapy (ERT). In the USA, it has become increasingly common to prescribe estrogens in combination with progestins since the early 1980s. An estimated 45% of menopausal US women aged 25-74 years in the early 1970s reported ever using HRT. Of those reporting HRT use in 1992, 31% reported taking progestins [1]. Use of progestins began earlier in Scandinavian countries than in the USA [2].Assessing breast cancer risk associated with HRT is complicated by the fact that many different hormones, regimens, and routes of administration have been used. During the 1980s the most common type of estrogenprogestin replacement therapy (EPRT) in the USA consisted of estrogens administered for the first 21-25 days of the calendar month and progestins added cyclically during the last 10-14 days of estrogen treatment. Other regimens, including continuous daily treatment with both estrogens and progestins, were developed to avoid the withdrawal bleeding that many women experience with cyclic therapy [3]. More recently, new regimens were introduced to prevent or minimize the breakthrough bleeding that is common during the first months of combined/ continuous EPRT. These include the use of progestins only every second or third month AbstractProgestins are included in menopausal hormone replacement therapy to counteract the increased risk for endometrial cancer associated with estrogen replacement therapy. Studies of hormone replacement therapy and breast cancer risk and of changes in mammographic density according to different regimens of hormone replacement therapy suggest that, for the most part, estrogen-progestin replacement therapy has a more adverse effect on breast cancer risk than does estrogen replacement therapy. Many questions remain unresolved, however, including risk associated with different regimens of estrogen-progestin replacement therapy, and whether the effects vary according to tumor characteristics, such as histology, extent of disease, and hormone receptor status.

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Section: Hormone Replacement Therapy and Breast Cancer Risksupporting

confidence: 73%

Progesterone receptors - animal models and cell signaling in breast cancer: Implications for breast cancer of inclusion of progestins in hormone replacement therapies

Schairer

2002

Breast Cancer Res

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“…Previous studies have provided discrepant results regarding how the administration of progestins in EPT affects breast cancer risk, with some showing higher risks associated with continuous therapy (10, 14, 16, 21, 34, 45, 46, 54–56), another showed a higher risk associated with sequential therapy (15), and still others showing no major differences in the two regimens (9, 12, 13, 18, 29, 47). We found somewhat stronger associations for continuous than sequential EPT use, particularly for current and long-term use.…”

Section: Discussionmentioning

confidence: 99%

“…Numerous studies have reported stronger hormone associations for invasive lobular than ductal tumors tumors (9–13, 25, 27, 29–34). Few epidemiological studies, however, have been able to assess associations according to newer diagnostic criteria which incorporate classification of mixed ductal-lobular carcinomas as well as the more conventional categories of ductal and lobular tumors.…”

Section: Discussionmentioning

confidence: 99%

“…Increasing evidence suggests that hormone associations may be dependent on tumor characteristics, including stage or grade (24–26), histology (9–13, 25, 27–34) and hormone receptor status (12, 19, 24, 26, 27, 33–35), although results have not been entirely consistent. While most studies show that hormone associations are generally stronger for tumors with favorable clinical characteristics, WHI showed the reverse (36).…”

Section: Introductionmentioning

confidence: 99%

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Menopausal Hormone Therapy and Breast Cancer Risk in the NIH-AARP Diet and Health Study Cohort

Brinton¹,

Richesson²,

Leitzmann

et al. 2008

Cancer Epidemiology, Biomarkers &Amp; Prevention

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Background: Results from the Women's Health Initiative trial raise new questions regarding the effects of estrogen therapy (ET) and estrogen plus progestin therapy (EPT) on breast cancer risk. Methods: We analyzed data from 126,638 females, ages 50 to 71 years at baseline, who completed two questionnaires (1995-1996 and 1996-1997) as part of the NIH-AARP Diet and Health Cohort Study and in whom 3,657 incident breast cancers were identified through June 30, 2002. Hormone-associated relative risks (RR) and 95% confidence intervals (CI) of breast cancer were estimated via multivariable regression models. Results: Among thin women (body mass index <25 kg/ m

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“…The other published works on this topic were based on case-control study designs,7-11,15-17 for which stratum-specific absolute risks are not observed. Nevertheless, we can evaluate departures from additivity by assessing the relative excess risk for interaction (RERI) 23.…”

Section: Discussionmentioning

confidence: 99%

Hormone Replacement Therapy, Family History, and Breast Cancer Risk Among Postmenopausal Women

et al. 2009

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Background Evidence is mixed regarding how familial predisposition to breast cancer affects the relation between hormone replacement therapy and risk of postmenopausal breast cancer. We investigated whether the risk difference for invasive breast cancer attributable to estrogen plus progesterone replacement therapy is greater among women with a first-degree family history of the disease. Methods This study is a longitudinal follow-up of 16,608 postmenopausal women aged 50–79 years who were enrolled between 1993 and 2002 in the Women’s Health Initiative randomized trial of estrogen plus progesterone replacement therapy versus placebo. Results Three hundred forty-nine cases of invasive breast cancer occurred during a mean follow-up period of 5.6 years. The invasive breast cancer risk difference attributable to the hormone therapy was 0.007 among women with first-degree family history and 0.005 among the others, resulting in a negligible interaction contrast (IC = 0.002; 95% confidence interval = −0.014 to 0.018). The interaction contrast restricted to estrogen-receptor-positive invasive breast cancers was also negligible (IC = −0.006; 95% CI = −0.021 to 0.008). Conclusion Family history and estrogen plus progesterone replacement therapy have independent and noninteracting effects on the risk of invasive breast cancer among participants in the Women’s Health Initiative randomized trial.

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Does Menopausal Hormone Replacement Therapy Interact With Known Factors to Increase Risk of Breast Cancer?

Abstract: We found no evidence that the risk of breast cancer associated with EPRT is limited to subgroups of women with specific cofactors. Tumors in EPRT users are more often hormone receptor--positive, indicating that they may have a better prognosis than breast cancer overall.

Cited by 58 publications

References 21 publications

Progesterone receptors - animal models and cell signaling in breast cancer: Implications for breast cancer of inclusion of progestins in hormone replacement therapies

Progesterone receptors - animal models and cell signaling in breast cancer: Implications for breast cancer of inclusion of progestins in hormone replacement therapies

Menopausal Hormone Therapy and Breast Cancer Risk in the NIH-AARP Diet and Health Study Cohort

Hormone Replacement Therapy, Family History, and Breast Cancer Risk Among Postmenopausal Women

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