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( Galanti et al . 1995 , Rossing et al . 2000 , Sakoda & Horn-Ross 2002 , Horn-Ross et al . 2011 ). In contrast, low dose of estrogen in contraceptives and in replacement therapy in postmenopausal women does not contribute to a higher risk of thyroid

Introduction There is ample experimental, epidemiological, and clinical evidence linking estrogens and breast cancer risk ( Henderson & Feigelson 2000 , Russo & Russo 2006 ). Several established risk factors for breast cancer are strongly

al. 2015 ) and are classified into subtypes according to the findings of histological, genetic and molecular analyses. Subtypes are defined according to the expression of estrogen (ER) or progesterone receptors (PR), with or without the expression of

interest in the effects of estrogen on the prostate gland. Initially, hormone treatment for prostate cancer involved manipulation of systemic hormone levels with exogenous estrogen therapy (in the form of high-dose diethylstilbestrol) to suppress androgen

of senescence during the development of tumors. In this study, we used a previously developed pituitary tumor experimental model, which consists of long-term estrogen administration in rats, and leads to the formation of prolactin (PRL) secretory

features, including similar SM cell types, expression of estrogen and progesterone receptors (ERs and PRs) ( Benassayag et al . 1999 ), and growth sensitivity to estrogens ( Maruo et al . 2004 ). In fact, a study on the uteri of ten LAM patients found

middle-aged patients ( van Kesteren et al . 1996 ). In MtF patients, development of female secondary sexual characteristics requires hormonal treatment with anti-androgens and estrogens. The doses of estrogens typically used in MtF patients are higher

Introduction Lymphangioleiomyomatosis (LAM) is a rare, devastating pulmonary lung disease almost exclusively affecting women in their reproductive years whereby estrogen-sensitive metastatic smooth-muscle cell-like adenomas grow within the

crosstalk between insulin and estrogen signaling pathways triggers multiple biological events in breast carcinogenesis ( Rose & Vona-Davis 2012 , Catsburg et al . 2014 ). Estrogens mainly act through the classical estrogen receptor α (ESR1) and β (ESR2

. Androgen deprivation therapy (ADT) has been a cornerstone of PCa management since the 1940s. A variety of approaches have been used: bilateral orchiectomy; high-dose oral or parenteral estrogens; luteinizing hormone-releasing hormone (LHRH) agonists (LHRHa