scholarly journals The role of sex steroid hormones, cytokines and the endocannabinoid system in female fertility

2011 ◽  
Vol 17 (3) ◽  
pp. 347-361 ◽  
Author(s):  
T. Karasu ◽  
T. H. Marczylo ◽  
M. Maccarrone ◽  
J. C. Konje
Keyword(s):  
Steroid Hormones ◽  
Endocannabinoid System ◽  
Sex Steroid Hormones ◽  
Female Fertility ◽  
Sex Steroid

scholarly journals Sex Steroid Hormones as a Balancing Factor in Oral Host Microbiome Interactions

2021 ◽  
Vol 11 ◽  
Author(s):  
Pilar Cornejo Ulloa ◽  
Bastiaan P. Krom ◽  
Monique H. van der Veen
Keyword(s):  
Oral Cavity ◽  
Steroid Hormones ◽  
Sex Steroid Hormones ◽  
Oral Microbiome ◽  
Host Cells ◽  
Sex Steroid ◽  
Hormonal Changes ◽  
Host Microbe Interactions ◽  
Oral Microorganisms

Sex steroid hormones (SSH) are cholesterol-derived molecules. They are secreted into saliva and enter the oral cavity, triggering physiological responses from oral tissues, with possible clinical implications, such as gingival inflammation and bleeding. SSH and hormonal changes affect not only oral host cells but also oral microorganisms.Historically, most research has focused on the effect of hormonal changes on specific bacteria and yeasts. Recently a broader effect of SSH on oral microorganisms was suggested. In order to assess the role of SSH in host-microbe interactions in the oral cavity, this review focuses on how and up to what extent SSH can influence the composition and behavior of the oral microbiome. The available literature was reviewed and a comprehensive hypothesis about the role of SSH in host-microbiome interactions is presented. The limited research available indicates that SSH may influence the balance between the host and its microbes in the oral cavity.

Role of sex steroid hormones in relative refractoriness to angiotensin II during pregnancy

1984 ◽  
Vol 149 (2) ◽  
pp. 177-183 ◽  
Author(s):  
Tsuneo Tamai ◽  
Shumpei Matsuura ◽  
Nobuya Tatsumi ◽  
Takaaki Nunotani ◽  
Norimasa Sagawa
Keyword(s):  
Angiotensin Ii ◽  
Steroid Hormones ◽  
Sex Steroid Hormones ◽  
Sex Steroid

scholarly journals Sex steroid hormones and risk of breast cancer incidence and survival: A two-sample Mendelian randomization study

2021 ◽  
Author(s):  
Aayah Nounu ◽  
Siddhartha P. Kar ◽  
Caroline L Relton ◽  
Rebecca C Richmond
Keyword(s):  
Breast Cancer ◽  
Steroid Hormones ◽  
Mendelian Randomization ◽  
Sex Steroid Hormones ◽  
Sex Steroid ◽  
Genome Wide Association Studies ◽  
Luminal A ◽  
Luminal B ◽  
Genetic Instruments

Background Breast cancer (BC) is the cancer with the highest incidence and mortality in women worldwide. Observational epidemiological studies suggest a positive association between testosterone, estradiol, dehydroepiandrosterone sulphate (DHEAS) and both pre- and post-menopausal BC. Since previous studies may be prone to bias and confounding, we used a two-sample Mendelian randomization (MR) analysis to investigate this association. Methods Genetic instruments for nine sex steroid hormones and sex hormone binding globulin (SHBG) were obtained from genome-wide association studies (GWAS) conducted in the UK Biobank (total testosterone (TT) N:230,454, bioavailable testosterone (BT) N: 188,507 and SHBG N: 189,473), The United Kingdom Household Longitudinal Study (DHEAS N: 9,722), the LIFE-Adult and LIFE-Heart cohorts (estradiol N: 2,607), the LIFE-Heart cohort only (androstenedione N: 711, aldosterone N: 685, progesterone N: 1,259 and 17-hydroxyprogesterone N: 711) and the CORtisol NETwork (CORNET) consortium (cortisol N: 25,314). GWAS summary statistics were also obtained from the Breast Cancer Association Consortium (BCAC) for overall BC risk (N: 122,977 cases and 105,974 controls) and BC mortality (96,661 BC cases and 7,697 BC-specific deaths). Subtype specific analysis were carried out for incidence of estrogen receptor (ER)+ BC, ER- BC, luminal A-like BC, luminal B-like BC, luminal B/HER2-negative-like BC, HER2-enriched-like BC, triple negative BC (TNBC) and BRCA1 mutated TNBC. Results Using an inverse-variance weighted (IVW) approach, we found that a standard deviation (SD) increase in TT, BT and estradiol increased the risk of overall BC (OR: 1.14, 95% CI: 1.09-1.21, OR: 1.19, 95% CI: 1.07-1.33 and OR: 1.03, 95% CI: 1.01-1.06, respectively) and ER+ BC (OR: 1.19, 95% CI: 1.12-1.27, OR: 1.25, 95% CI: 1.11-1.40 and OR: 1.06, 95% CI: 1.03-1.09, respectively). A SD increase in DHEAS also increased ER+ BC risk (OR: 1.09, 95% CI: 1.03-1.09). Subtype specific analyses showed similar associations with ER+ expressing subtypes: luminal A-like BC, luminal B-like BC and luminal B/HER2-negative-like BC. A SD increase in cortisol was associated with poor survival after a diagnosis of ER- BC (HR: 2.35, 95% CI: 1.00-5.49). Discussion/Conclusion TT, BT, DHEAS and estradiol increase the risk of ER+ type BCs similar to observational studies, but none of these hormone measures are associated with BC survival. We found some evidence that cortisol reduced ER- BC survival. Stronger genetic instruments are required before definitive conclusions can be made about the role of other sex-steroid hormones in breast cancer. Understanding the role of sex steroid hormones in BC risk, particularly subtype-specific risks, highlights the potential importance of attempts to modify and/or monitor hormone levels in order to prevent BC.

Sex steroid hormones in pairs of tumor and serum from breast cancer patients and pathobiological role of androstene-3β, 17β-diol

2011 ◽  
Vol 102 (10) ◽  
pp. 1848-1854 ◽  
Author(s):  
Naoko Honma ◽  
Shigehira Saji ◽  
Makiko Hirose ◽  
Shin-ichiro Horiguchi ◽  
Katsumasa Kuroi ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Patients ◽  
Steroid Hormones ◽  
Sex Steroid Hormones ◽  
Sex Steroid ◽  
Breast Cancer Patients
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