1.Elevation of C-reactive protein during the luteal phase in healthy adolescents.
Merino PM1, Martínez D, Iñiguez G, Lopez P, Cassorla F, Perez-Bravo F, Codner E. Gynecol Endocrinol. 2015 Apr;31(4):260-3. doi: 10.3109/09513590.2014.982086. Epub 2014 Nov 13.
INTRODUCTION: Variations in inflammatory markers have been reported in adult women during the luteal phase, but whether these findings are observed during adolescence is unknown. We postulate that higher ultrasensitive C-reactive protein (usCRP) and lower 2-hydroxyestrone (2OHE) levels, an estrogen metabolite with cardioprotective actions, are present during the luteal phase in young women.
2.Relationships of sex steroid hormone levels in benign and cancerous breast tissue and blood: A critical appraisal of current science.
Stanczyk FZ1, Mathews BW2, Sherman ME3. Steroids. 2015 Jul;99(Pt A):91-102. doi: 10.1016/j.steroids.2014.12.011. Epub 2014 Dec 30.
A systematic review of the literature on sex steroid measurement in breast tissue identified only 19 articles meeting the following criteria: menopausal status given; steroids measured in tissue homogenates by conventional RIA with a purification step or by mass spectrometry; and values reported per g tissue or per g protein. Twelve articles were analyzed in detail for: ratios of sex steroid hormone levels in cancerous or benign tissues to blood levels, stratified by menopausal status; ratios between the different hormone levels within tissues or within blood; and difference in these ratios between tissue and blood compartments. Estrogen and androgen concentrations varied greatly in benign and cancerous tissues and in blood between individuals. Postmenopausal, but not premenopausal, estradiol concentrations were significantly higher in cancerous compared to benign breast tissue. The estradiol/estrone ratio was lowest in premenopausal benign tissue, and substantially higher in premenopausal cancerous tissue and postmenopausal benign and cancerous tissues.
3.Estrogen Metabolism and Risk of Postmenopausal Endometrial and Ovarian Cancer: the B∼FIT Cohort.
Dallal CM1,2, Lacey JV Jr3, Pfeiffer RM4, Bauer DC5,6, Falk RT7, Buist DS8, Cauley JA9, Hue TF6, LaCroix AZ10, Tice JA5, Veenstra TD11,12, Xu X12, Brinton LA7; B∼FIT Research Group. Horm Cancer. 2016 Feb;7(1):49-64. doi: 10.1007/s12672-015-0237-y. Epub 2016 Jan 4.
Estrogen metabolites may have different genotoxic and mitogenic properties yet their relationship with endometrial and ovarian cancer risk remains unclear. Within the Breast and Bone Follow-up to the Fracture Intervention Trial (B∼FIT, n = 15,595), we conducted a case-cohort study to evaluate 15 pre-diagnostic serum estrogens and estrogen metabolites with risk of incident endometrial and ovarian cancer among postmenopausal women not on hormone therapy. Participants included 66 endometrial and 67 ovarian cancer cases diagnosed during follow-up (∼10 years) and subcohorts of 346 and 416 women, respectively, after relevant exclusions. Serum concentrations were measured by liquid chromatography-tandem mass spectrometry. Hazard ratios (HRs) and 95 % confidence intervals (CIs) were estimated using Cox proportional hazard regression. Exposures were categorized in tertiles (T) and analyzed individually, as metabolic pathways (C-2, -4, or -16) and as ratios to parent estrogens (estradiol, estrone).
4.Glucuronidation of estrone and 16α-hydroxyestrone by human UGT enzymes: The key roles of UGT1A10 and UGT2B7.
Kallionpää RA1, Järvinen E1, Finel M2. J Steroid Biochem Mol Biol. 2015 Nov;154:104-11. doi: 10.1016/j.jsbmb.2015.07.013. Epub 2015 Jul 26.
The glucuronidation of estrone and 16α-hydroxyestrone by recombinant human UDP-glucuronosyltransferase enzymes (UGTs) of subfamilies 1A, 2A and 2B was studied. Microsomes from human liver and small intestine were also tested for the glucuronidation of these two estrogens. The results revealed that UGT1A10 is by far the most active enzyme in estrone glucuronidation. UGT1A10 also exhibited high rate of 16α-hydroxyestrone conjugation at the 3-OH, whereas UGT2B7 catalyzed its glucuronidation at high rates at the 16-OH. Human liver microsomes exhibited high rates of 16α-hydroxyestrone-16-glucuronide formation, but very low formation rates of either 16α-hydroxyestrone-3-glucuronide or estrone glucuronide. On the other hand, human intestine microsomes catalyzed the formation of all these 3 different glucuronides at high rates. Kinetic analyses revealed very low Km value for 16α-hydroxyestrone glucuronidation by UGT2B7, below 4 μM, suggesting higher affinity than commonly found among UGTs and their substrates.