Sex Hormone-Binding Globulin (SHBG), estradiol and breast cancer

Fortunati, Nicoletta; Catalano, Maria Graziella; Boccuzzi, Giuseppe; Frairia, Roberto

doi:10.1016/j.mce.2009.09.012

Cited by 98 publications

(72 citation statements)

References 101 publications

(80 reference statements)

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“…The second approach has the effect of increasing any FEI that is based on an undetectable E 2 by 60 % compared to the first. The fact that neither approach was any stronger than total E 2 as a predictor of fracture suggests either that FEI provides a poor estimate of bioavailable E 2 or that SHBG has an additional influence on bone other than its E 2 binding effect [26,27]. Our results are supported by the population-based study from Rotterdam, where free E 2 and non-SHBG-bound E 2 were calculated by the method of Sodergard et al [28].…”

Section: Discussionsupporting

confidence: 57%

Endogenous Estradiol and The Risk of Incident Fracture in Postmenopausal Women: The OPUS Study

et al. 2012

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Some, but not all, studies have found that low endogenous estradiol levels in postmenopausal women are predictive of fractures. The aim of this study was to examine the roles of endogenous estradiol (E(2)), sex hormone binding globulin (SHBG), and dehydroepiandrosterone sulfate (DHEAS) in the prediction of incident vertebral and nonvertebral fractures. The study subjects were 797 postmenopausal women from the population-based OPUS (Osteoporosis and Ultrasound Study) study. Spine radiographs and dual-energy X-ray absorptiometry scans were obtained for all subjects at baseline and 6-year follow-up. Nonfasting blood samples were taken at baseline for E(2), SHBG, DHEAS, and bone turnover markers. Incident nonvertebral fractures were self-reported and verified; vertebral fractures were diagnosed at a single center from spinal radiographs. Medical and lifestyle data were obtained by questionnaire at each visit. Thirty-nine subjects had an incident vertebral fracture and 119 a nonvertebral fracture. Estradiol in the lowest quartile predicted vertebral fracture independent of confounders including age, body mass index, bone mineral density, bone turnover, fracture history, and use of antiresorptive therapy, with an OR of 2.97 (95 % confidence interval [CI] 1.52-5.82) by logistic regression. A calculated free estradiol index was not a stronger predictor than total E(2). Higher SHBG predicted vertebral fracture independently of age and body mass index, but not independently of E(2), bone mineral density, or prevalent fracture. Low DHEAS did not predict vertebral fracture. Nonvertebral fractures were not predicted by any of E(2), SHBG, or DHEAS, either in univariate or multivariate analyses. These findings suggest that there may be mechanistic differences in the protective effect of E(2) at vertebral compared with nonvertebral sites.

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Section: Discussionsupporting

confidence: 57%

Endogenous Estradiol and The Risk of Incident Fracture in Postmenopausal Women: The OPUS Study

et al. 2012

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“…Low SHBG level implies higher bioavailability of estrogens and may indicate higher levels of insulin or insulinlike growth factor-1 (26). A direct inhibitory role of SHBG on breast cancer cell proliferation has also been proposed (27).…”

Section: Discussionmentioning

confidence: 99%

Endogenous Sex Steroids and Risk of Cervical Carcinoma: Results from the EPIC Study

Rinaldi

Plummer

Biessy

et al. 2011

Cancer Epidemiology, Biomarkers &Amp; Prevention

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Background: Epidemiologic data and animal models suggest that, despite the predominant role of human papillomavirus infection, sex steroid hormones are also involved in the etiology of invasive cervical carcinoma (ICC).Methods: Ninety-nine ICC cases, 121 cervical intraepithelial neoplasia grade 3 (CIN3) cases and 2 control women matched with each case for center, age, menopausal status and blood collection-related variables, were identified in the European Prospective Investigation into Cancer and Nutrition (EPIC) study. Circulating levels of testosterone (T) and estradiol (E 2 ); dehydroepiandrosterone sulfate (DHEAS); progesterone (premenopausal women); and sex hormone-binding globulin (SHBG) were measured using immunoassays. Levels of free (f) T and E 2 were calculated from absolute concentrations of T, E 2 , and SHBG. Odds ratios (ORs) and 95% confidence intervals (CI) were computed using regularized conditional logistic regression.Results: Among premenopausal women, associations with ICC were observed for fT (OR for highest vs. lowest tertile ¼ 5.16, 95% CI, 1.50-20.1). SHBG level was associated with a significant downward trend in ICC risk. T, E 2 , fE 2, and DHEAS showed nonsignificant positive association with ICC. Progesterone was uninfluential. Among postmenopausal women, associations with ICC were found for T (OR ¼ 3.14; 95% CI, 1.21-9.37), whereas E 2 and fT showed nonsignificant positive association. SHBG level was unrelated to ICC risk in postmenopausal women. No associations between any hormone and CIN3 were detected in either pre-or postmenopausal women.Conclusions: Our findings suggest for the first time that T and possibly E 2 may be involved in the etiology of ICC.Impact: The responsiveness of cervical tumors to hormone modulators is worth exploring. Cancer Epidemiol Biomarkers Prev; 20(12); 2532-40. Ó2011 AACR.

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“…Body fatness directly affects levels of many circulating hormones, such as insulin, insulin-like growth factors, oestrogens and inflammatory factors, which are all wellknown risk factors for BC risk [18,19,36,[38][39][40], thus creating an environment that encourages carcinogenesis and discourages apoptosis. For these reason we performed also a regression analysis to investigate the possible impact of PRKA gene polymorphic variants on BMI.…”

Section: Discussionmentioning

confidence: 99%

Variation in genes coding for AMP-activated protein kinase (AMPK) and breast cancer risk in the European Prospective Investigation on Cancer (EPIC)

Campa

Claus

Dostal

et al. 2010

Breast Cancer Res Treat

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AMP-activated protein kinase (AMPK) is an energy sensing/signalling intracellular protein which is activated by an increase in the cellular AMP:ATP ratio after ATP depletion. Once activated, AMPK inhibits fatty acid synthesis and the Akt-mTOR pathway, and activates the p53-p21 axis. All these molecular mechanisms are thought to play a key role in breast carcinogenesis. We investigated the genetic variability of four genes encoding AMPK (PRKAA1, PRKAA2, PRKAB1 and PRKAB2). Using a tagging approach and selecting SNPs we covered all the common genetic variation of these genes. We tested association of tagging SNPs in our four candidate genes with breast cancer (BC) risk in a study of 1340 BC cases and 2536 controls nested into the European Prospective Investigation into Cancer and Nutrition (EPIC). Given the relevance of AMPK on fatty acid synthesis and the importance of body fatness as a BC risk factor, we tested association of SNPs and body-mass index as well. We observed no statistically significant association between the SNPs in the PRKAs genes and BC risk and BMI after correction for multiple testing.

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Sex Hormone-Binding Globulin (SHBG), estradiol and breast cancer

Cited by 98 publications

References 101 publications

Endogenous Estradiol and The Risk of Incident Fracture in Postmenopausal Women: The OPUS Study

Endogenous Estradiol and The Risk of Incident Fracture in Postmenopausal Women: The OPUS Study

Endogenous Sex Steroids and Risk of Cervical Carcinoma: Results from the EPIC Study

Variation in genes coding for AMP-activated protein kinase (AMPK) and breast cancer risk in the European Prospective Investigation on Cancer (EPIC)

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