Dataset Information

Impact of Hormone Replacement Therapy on Risk of Ovarian Cancer in Postmenopausal Women with De Novo Endometriosis or a History of Endometriosis.

ABSTRACT: The effect of hormone replacement therapy (HRT) on the malignant transformation of postmenopausal endometriosis remains unclear. This study aimed to investigate the impact of HRT on ovarian cancer occurrence in postmenopausal women with de novo endometriosis or a history of endometriosis. A total of 10,304 women that received HRT (the HRT group) and 10,304 that did not (the control group) were selected by 1:1 matching those that met the study criteria. Incidences of ovarian cancer (0.3% in the HRT group and 0.5% in the control group) and cumulative incidence rates of ovarian cancer were similar in the two groups. The overall mean duration of HRT was 1.4 ± 2.2 years, but the duration of HRT in women with ovarian cancer was 2.2 ± 2.9 years. After adjusting for co-variables, receipt of HRT, duration of HRT, combined use of estrogen and progesterone, and tibolone were not found to be risk factors for ovarian cancer. However, the use of estrogen alone was found to be a significant risk factor for ovarian cancer (HR 2.898; 95% CI 1.251-6.715; p = 0.013). With the exception of HRT using estrogen alone, HRT did not increase the risk of ovarian cancer in postmenopausal women with a history of endometriosis or de novo endometriosis.

SUBMITTER: Lee HJ

PROVIDER: S-EPMC10046182 | biostudies-literature | 2023 Mar

REPOSITORIES: biostudies-literature

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Impact of Hormone Replacement Therapy on Risk of Ovarian Cancer in Postmenopausal Women with De Novo Endometriosis or a History of Endometriosis.

Lee Hee Joong HJ Lee Banghyun B Choi Hangseok H Kim Taehee T Kim Yejeong Y Kim Yong Beom YB

Cancers 20230310 6

The effect of hormone replacement therapy (HRT) on the malignant transformation of postmenopausal endometriosis remains unclear. This study aimed to investigate the impact of HRT on ovarian cancer occurrence in postmenopausal women with de novo endometriosis or a history of endometriosis. A total of 10,304 women that received HRT (the HRT group) and 10,304 that did not (the control group) were selected by 1:1 matching those that met the study criteria. Incidences of ovarian cancer (0.3% in the H ...[more]

PMID: 36980597

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Project description:Title: Transcriptome analysis of human endometrial tissues from healthy post-menoupausal women reflecting the endometrial response to 3-weeks treatment with tibolone, E2 and E2+MPA. In an observational, open, non-randomized, controlled study uterine tissues were collected in order to generate endometrial gene expression profiles. healthy postmenopausal women were enrolled into the following treatment groups: Control-group; Tibolone-group, 2,5 mg of tibolone (administered orally) every day, starting 21 days prior to surgery; Estradiol-group, 2 mg of estradiol (administered orally) every day, starting 21 days prior to surgery; Estradiol+progestagen-group, 2 mg of estradiol (administered orally) and 5 mg of MPA (Medroxy Progesteroneacetate, administered orally) every day, starting 21 days prior to surgery. Pure (100%) endometrium was isolated from the snap-frozen uterine tissues and used for RNA isolation. RNA was labeled and hybridized to whole genome Affymetrix U133plus2 GeneChips containing 54,614 probe sets, representing approximately 47,000 transcripts. Relative to the control group, 940 genes are regulated in the endometrium of E2 treated patients, whereas only 198 genes are significantly regulated in endometria from tibolone or E2+MPA treated patients. Furthermore, only 9% of E2 regulated genes are also regulated by tibolone (85 out of 940), only 5% are also regulated by E2+MPA treatment and the overlap between tibolone and E2+MPA treatment is about 10%. This indicated that tibolone-treatment results in a weak endometrial profile similarity to E2 treatment and no profile similarity to E2+MPA treatment. A more detailed analysis showed that down stream processes, such as regulation of the cell cycle, angiogenesis and cell proliferation are almost not affected by tibolone treatment but, in contrast, are significantly affected by E2. For example, upon staining with Ki67, a marker for mitotic activity, significantly increased stromal as well as glandular cell proliferation was observed in the endometria from the E2-only treated group, while tibolone treatment resulted only in a slight increase in stromal cell proliferation (and no increase in glandular cell proliferation). These results indicate that in contrast to long-term tibolone use, short-term (21-days) use results in some estrogenic stimulation of the endometrium, which is clearly far less and rather different from what is observed during E2 treatment. References: Klaassens et al., 2006 Hanifi-Moghaddam et al., 2007 Verheul et al., 2007

Project description:ImportanceMenopausal hormone therapy (MHT) is the treatment of choice for symptoms of menopause. However, its adoption is hindered by the risk-benefit trade-off in relation to acute and chronic diseases.ObjectiveTo evaluate trends in and correlates of MHT use among postmenopausal women in the US from 1999 to March 2020.Design, setting, and participantsThis serial cross-sectional analysis of MHT use used data from the nationally representative National Health and Nutrition Examination Survey (NHANES). Participants included noninstitutionalized US postmenopausal women from 10 NHANES study cycles (1999-2000 to 2017-March 2020 [pre-COVID-19 pandemic]). Data were analyzed from December 2023 to April 2024.ExposuresNHANES study cycle.Main outcomes and measuresPrevalence of MHT use was extracted from the prescription medication data collected during NHANES household interviews. MHT formulations were determined by hormone type.ResultsData on 13 048 US postmenopausal women (47.1% ≥65 years old) were analyzed. From 1999 to 2020, the prevalence of MHT use decreased among women of all age groups, from 26.9% (95% CI, 22.6%-31.7%) in 1999 to 4.7% (95% CI, 3.4%-6.5%) in 2020. Until 2002, MHT use was highest among women aged 52 to 65 years, but since 2005, MHT use has been highest among women younger than 52 years. MHT use decreased by 23.5% (95% CI, 11.4%-35.6%), 31.4% (95% CI, 23.4%-39.5%), and 10.6% (95% CI, 6.3%-14.8%) for women younger than 52 years, 52 years to younger than 65 years, and 65 years and older, respectively. Prevalence of MHT use decreased from 13.8% (95% CI, 8.5%-21.7%) to 2.6% (95% CI, 1.5%-4.6%) for Hispanic women, 11.9% (95% CI, 8.5%-16.3%) to 0.5% (95% CI, 0.2%-1.1%) for non-Hispanic Black women, and 31.4% (95% CI, 27.1%-36.1%) to 5.8% (95% CI, 4.1%-8.2%) for non-Hispanic White women. Non-Hispanic White women consistently had the highest prevalence of MHT use. Estrogen-only formulation accounted for more than 50% of the MHT for most study periods. The prevalence of MHT use varied by family income-to-poverty ratio, health insurance coverage in all racial and ethnic groups, weight, and smoking status among non-Hispanic White women, as well as by education attainment among non-Hispanic Black and Hispanic women.Conclusions and relevanceResults of this cross-sectional study show that over the past 2 decades, MHT use declined among US postmenopausal women of all age and racial and ethnic groups. Women of racial and ethnic minority groups had lower prevalence of MHT use compared to non-Hispanic White women.

Project description:Risk assessment of future breast cancer risk through exposure to sex steroids currently relies on clinical scorings such as mammographic density. Knowledge about the gene expression patterns in existing breast cancer tumors may be used to identify risk factors in the breast tissue of women still free of cancer. The differential effects of estradiol, estradiol together with gestagens, or tibolone on breast cancer-related gene expression in normal breast tissue samples taken from postmenopausal women may be used to identify gene expression profiles associated with a higher breast cancer risk. Breast tissue samples were taken from 33 healthy postmenopausal women both before and after a six month treatment with either 2mg micronized estradiol [E2], 2mg micronized estradiol and 1mg norethisterone acetate [E2+NETA], 2.5mg tibolone [T] or [no HRT]. Except for [E2], which was only given to women after hysterectomy, the allocation to each of the three groups was randomized. The expression of 102 mRNAs and 46 microRNAs putatively involved in breast cancer was prospectively determined in the biopsies of 6 women receiving [no HRT], 5 women receiving [E2], 5 women receiving [E2+NETA], and 6 receiving [T]. Using epithelial and endothelial markers genes, non-representative biopsies from 11 women were eliminated. Treatment of postmenopausal women with [E2+NETA] resulted in the highest number of differentially (p<0.05) regulated genes (16.2%) compared to baseline, followed by [E2] (10.1%) and [T] (4.7%). Among genes that were significantly down-regulated by [E2+NETA] ranked estrogen-receptor-1 (ESR1, p=0.019) and androgen receptor (AR, p=0.019), whereas CYP1B1, a gene encoding an estrogen-metabolizing enzyme, was significantly up-regulated (p=0.016). Mammary cells triggered by [E2+NETA] and [E2] adjust for steroidogenic up-regulation through down-regulation of the estrogen-receptor pathway. In this prospective study, prolonged administration of [E2+NETA] and to a lesser extent of [E2] but not [T] were associated in otherwise healthy breast tissue with a change in the expression of genes putatively involved in breast cancer. Our data suggest that normal mammary cells triggered by [E2+NETA] adjust for steroidogenic up-regulation through down-regulation of the estrogen-receptor pathway. This feasibility study provides the basis for whole genome analyses to identify novel markers involved in increased breast cancer risk.

Dataset Information

Impact of Hormone Replacement Therapy on Risk of Ovarian Cancer in Postmenopausal Women with De Novo Endometriosis or a History of Endometriosis.

Publications

Impact of Hormone Replacement Therapy on Risk of Ovarian Cancer in Postmenopausal Women with De Novo Endometriosis or a History of Endometriosis.

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