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E E Connor, D L Wood, T S Sonstegard, A F da Mota, G L Bennett, J L Williams, and A V Capuco

Summary of linkage mapping of bovine steroid receptors estrogen receptor alpha (ERα), estrogen receptor beta (ERβ), progesterone receptor (PR), and estrogen-related receptor alpha (ERRα) Accession no. SNP* Chromosome Nearest marker 2-pt LOD Recombination

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Susana I Sá and Bruno M Fonseca

division of the VMN (VMNvl) expresses estrogen receptor (ER) a and b and progesterone receptors (PRs), which depend on the levels of their cognate ligands ( Lauber et al . 1990 , Shughrue et al . 1992 , Sá et al . 2013 , 2015 ). Earlier studies have

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J Varayoud, J G Ramos, L Monje, V Bosquiazzo, M Muñoz-de-Toro, and E H Luque

. Ramos JG , Varayoud J, Bosquiazzo V, Luque EH & Muñoz-de-Toro M 2002 Cellular turnover in the rat uterine cervix and its relationship to estrogen and progesterone receptor dynamics. Biology of Reproduction 67 735 –742

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Soyoung Choi, Hyejin Shin, Haengseok Song, and Hyunjung Jade Lim

blood vessels. Many uterine functions are under the regulation of ovarian steroid hormones, estrogens and progesterone (P 4 ; Dey et al . 2004 , Das 2009 ), and uterine cell types respond to hormones in a differential manner. Ovarian estrogen targets

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RA Medina, AM Meneses, JC Vera, C Guzman, F Nualart, F Rodriguez, M de los Angeles Garcia, S Kato, N Espinoza, C Monso, A Carvajal, M Pinto, and GI Owen

Estrogen replacement therapy and other unopposed estrogen treatments increase the incidence of endometrial abnormalities, including cancer. However, this effect is counteracted by the co-administration of progesterone. In the endometrium, glucose transporter (GLUT) expression and glucose transport are known to fluctuate throughout the menstrual cycle. Here, we determined the effect of estrogen and progesterone on the expression of GLUT1-4 and on the transport of deoxyglucose in Ishikawa endometrial cancer cells. Cells were incubated with estrogen, progesterone or combined estrogen and progesterone for 24 h and the effect on the expression of GLUT1-4 and on deoxyglucose transport was determined. We show that GLUT1 expression is upregulated by estrogen and progesterone individually, but that combined estrogen and progesterone treatment reverses this increase. Hormonal treatments do not affect GLUT2, GLUT3 or GLUT4 expression. Transport studies demonstrate that estrogen increases deoxyglucose transport at Michaelis-Menten constants (Kms) corresponding to GLUT1/4, an effect which disappears when progesterone is added concomitantly. These data demonstrate that different hormonal treatments differentially regulate GLUT expression and glucose transport in this endometrial cancer cell line. This regulation mirrors the role played by estrogen and progesterone on the incidence of cancer in this tissue and suggests that GLUT1 may be utilized by endometrial cancer cells to fuel their demand for increased energy requirement.

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L Sivaraman, SG Hilsenbeck, L Zhong, J Gay, OM Conneely, D Medina, and BW O'Malley

An early single full-term pregnancy induces a long-lasting protective effect against mammary tumor development in humans and rodents. This protective effect can be mimicked in rats by short-term administration of estrogen and progesterone hormones prior to carcinogen administration. The hormones of pregnancy are able to induce a proliferative block upon carcinogen challenge that is not observed in the age-matched virgin. We wished to determine whether carcinogen is needed to induce a paracrine-to-autocrine shift of proliferation in steroid receptor positive cells or if such a cell population already exists in the age-matched virgin mammary gland. Here we show that estrogen receptor positive (ER+) proliferating cells are rare in the developing mammary gland of the virgin rat but represent the majority of the proliferating cells in the mature (96-day-old) mammary gland of the virgin rat. As the majority of the proliferating cells before carcinogen challenge were ER positive, the ER+ proliferating cells in the mature mammary gland may represent the target cells for carcinogen-induced transformation. Importantly, prior exposure of the mammary gland to pregnancy levels of estrogen/progesterone blocked this positive association. This ability to block the proliferation of the ER+ cells may be one factor by which pregnancy induces protection against breast cancer.

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W Imagawa and VK Pedchenko

Mammary gland development is regulated by complex interactions among mammogenic hormones and locally derived paracrine growth factors. In epithelial tissues, keratinocyte growth factor (KGF or FGF-7) originates in the stroma while its receptor (KGFR or FGFR2-IIIb) is present only in the epithelium. Previous work showed that estrogen but not progesterone could stimulate the synthesis of KGF in mammary stroma in vivo. The effects of 17 beta-estradiol and progesterone on KGFR expression in vivo were examined in these studies. Peripubertal and mature virgin mice received subcutaneous injections of hormone in sesame oil after which KGFR mRNA levels were assayed by ribonuclease protection analysis of mammary gland RNA. Estradiol treatment caused a dose- and time-dependent decrease in KGFR mRNA level in mice from both age groups while stimulating ductal growth after 7 days of treatment. Inhibition of KGFR expression was near maximal at an estradiol dose of 2 microg after 1 day of treatment. Progesterone injection increased KGFR mRNA levels but this effect correlated with the stimulation of ductal growth. However, when progesterone was co-administered with estradiol, KGFR mRNA levels were maintained in the absence of any effect on ductal growth. Thus, estradiol inhibited KGFR mRNA only when elevated unopposed by progesterone. These data show that KGFR expression is determined by the ratio of estradiol and progesterone and suggests a mechanism through which these hormones can co-operate to optimize their growth-promoting effects. Consequences of hormone imbalance are also implicated.

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Josephine F Trott, Katherine C Horigan, Julia M Gloviczki, Kristen M Costa, Bradley A Freking, Chantal Farmer, Kanako Hayashi, Thomas Spencer, Joseph E Morabito, and Russell C Hovey

gilts following hormone treatment. Ovary-intact nulliparous gilts were treated for 3 d with saline, estrogen (E 2 ), or progesterone (P). Total RNA was DNAse-treated and analyzed for the level of p PRLR -LF mRNA by quantitative RT-PCR with normalization

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Charlotta Dabrosin

difference in estradiol levels between breast tissue and subcutaneous fat. Plasma progesterone correlated significantly with local breast tissue estradiol. Together these results suggest that progesterone affects the local conversion of estrogens in normal

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S Jang and L S H Yi

presence of a functional progesterone receptor, we performed the ligand blot assay. When the specificity of interaction was evaluated by binding competitions with unlabeled progesterone, progesterone antagonist RU486 or estrogen, unlabeled progesterone and