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Indrajit Chowdhury, Kelwyn Thomas, Anthony Zeleznik and Winston E Thompson

450scc), 3β-hydroxysteroid dehydrogenase (3β-HSD), and aromatase ( cyp19a1 ) ( Miller & Bose 2011 ). All steroidogenic pathways begin in the mitochondria, where regulation of the cellular steroidogenic capacity occurs through key enzymatic rate

Open access

Douglas A Gibson, Paul A Foster, Ioannis Simitsidellis, Hilary O D Critchley, Olympia Kelepouri, Frances Collins and Philippa T K Saunders

et al . 2016 b ). Importantly, we have established that expression of CYP19A1 (aromatase, the key enzyme required for conversion of androgens to estrogens) as well as AKR1C3 and SRD5A1 (enzymes that convert precursor androgens into

Open access

J M Young and A S McNeilly

development reaches the preovulatory stage ( Young & McNeilly 2010 ). Before the expression of aromatase in granulosa cells, follicles are exposed to varying levels of androgens derived from thecal cells largely under the control of LH. In vitro , testosterone

Open access

T Traboulsi, M El Ezzy, J L Gleason and S Mader

development have led to the development and clinical use of small synthetic molecules that block either estrogen production (aromatase inhibitors) or estrogenic signaling (antiestrogens, AEs). AEs are steroids or steroid mimics that compete with endogenous

Open access

Ross S Thomas, Naveed Sarwar, Fladia Phoenix, R Charles Coombes and Simak Ali

response to anti-estrogens, such as tamoxifen ( Osborne 1998 ), and to aromatase inhibitors that inhibit estrogen biosynthesis ( Henderson & Piccart-Gebhart 2005 ), demonstrating the importance of ERα in breast cancer progression. However, a proportion of