The Journal of Steroid Biochemistry and Molecular Biology
Local and peripheral aromatase and breast cancerControl of aromatase activity in breast cancer cells: The role of cytokines and growth factors☆
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Central aromatization: A dramatic and responsive defense against threat and trauma to the vertebrate brain
2020, Frontiers in NeuroendocrinologyCitation Excerpt :PGE2 has a high affinity for four known E-prostanoid (EP) receptors: EP 1–4 (Singh et al., 1997). Binding of PGE2 to these receptors can regulate aromatase and E2 via modulation of downstream signaling pathways in other systems (Duncan and Saldanha, 2011; Phillips et al., 1978; Reed et al., 1993). Surprisingly, EP-1 and EP-2 receptors were not represented in the zebra finch genome, however they may play a greater role in non-avian species for the purpose of this review we are going to focus on EP-3 and EP-4 (Warren et al., 2010).
Induction of Estrogen Response Following Injury
2015, Estrogen Effects on Traumatic Brain Injury: Mechanisms of Neuroprotection and RepairTraumatized and inflamed - But resilient: Glial aromatization and the avian brain
2013, Hormones and BehaviorCitation Excerpt :The hypothesis that an alternate promoter may be responsible for the induction of glial aromatase led us to identify factors associated with neurotrauma that are also known to activate aromatase promoters. Cytokines, a major class of signals up-regulated by traumatic brain injury regulate aromatase gene expression via alternate promoters in normal and malignant breast tissue (Purohit et al., 1995, 2005; Reed et al., 1993; Singh et al., 1997) and microinjections of cytokines into a rat stab wound significantly increase gliosis (Ghirnikar et al., 1998). We therefore reasoned, that cytokine expression may be associated with the up-regulation of glial aromatase in the songbird brain.
Aromatase, breast cancer and obesity: A complex interaction
2012, Trends in Endocrinology and MetabolismCitation Excerpt :These groups demonstrated significantly elevated levels of estrone, estrone sulfate and estradiol in breast tumor tissue compared with circulating levels [52–54]. Several groups consistently found increased aromatase enzyme activity and mRNA levels in breast fat adjacent to the cancer tissue compared with distal fat or disease-free breast adipose tissue [17,21,45,46,55–57]. In vivo evidence from a transgenic mouse model revealed that aromatase overexpression in breast tissue was sufficient for maintaining hyperplasia in the absence of circulating estrogen and that aromatase inhibitors abrogated hyperplasia [58].
Molecular endocrinology and breast cancer - A reed before the wind lives on (a tribute to Professor Mike Reed)
2011, SteroidsCitation Excerpt :Papers were published on plasma levels of oestrogen in women with and without breast cancer [13], endogenous oestrogen production and metabolism in women with breast or endometrial cancer [14,15], and metabolic clearance rates of oestrogen [14]. A logical extension was to elucidate the role of growth factors and cytokines in the regulation of key enzymes of steroid metabolic pathways [16–20]. More recently Mike became involved in the development of enzyme inhibitors and exploring endocrine-cytotoxic therapy for cancers [21–24].
Aromatase and COX in breast cancer: Enzyme inhibitors and beyond
2007, Journal of Steroid Biochemistry and Molecular Biology
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Proceedings of the Third International Aromatase Conference.Basic and Clinical Aspects of Aromatase, Bologna, Italy, 14–17 June 1992.