Ed two models. Model 1 was constructed using variables with P
Ed two models. Model 1 was constructed using variables with P
Test for trends. The Cox proportional hazards regression model was used to control for multiple factors simultaneously and to estimate adjusted hazard ratios (HRs) and 95 confidence intervals. The relative increase in the risk of breast cancer recurrence for each of the three higher quartiles was estimated in comparison to that for the lowest quartile; it was also used to test for a linear trend
Early breast cancer. The patients described in thisSieuwerts et al. Breast Cancer Research 2010, 12:R103 http://breast-cancer-research.com/content/12/6/RPage 7 ofTable 3 Disease-free survival, metastasis-free survival, and overall survival as a function of continuous DC-SCRIPT in lymph node-negative diseaseAssociation with continuous DC-SCRIPT Cohort Lymph node-negative ESR1 mRNA-negativea ESR1 mR
Tion-inducing activities of ESR1 [1,2]. Unraveling the precise role of DC-SCRIPT in the complex genomic and non-genomic interplay between ESR1, ESR2, and their isoforms [21-23] might turn out to be rewarding for elucidating the `yin-yang' role of these factors in breast cancer. As DC-SCRIPT can inhibit ERa and PR activity, a second aim of the study was to address whether DCSCRIPT affects the respo
Receptor modulation and prognostic significance in primary breast cancer. J Natl Cancer Inst 2010, 102:54-68. 8. Ramadoss P, Marcus C, Perdew GH: Role of the aryl hydrocarbon receptor in drug metabolism. Expert Opin Drug Metab Toxicol 2005, 1:9-21. 9. Osborne CK, Schiff R, Fuqua SA, Shou J: Estrogen receptor: current understanding of its activation and modulation. Clin Cancer Res 2001, 7:4338s-434
F 1.9 . The homeostasis model assessment for insulin resistance (HOMA-IR) was used to estimate insulin resistance as determined by the following formula: ((fasting insulin (U/mL) ?fasting glucose (mmol/liter))/22.5 [24]. Serum estradiol was measured using an electrochemiluminescence immunoassay analyzer (Roche Modular Analytics E170; Roche, Mannheim, Germany) with a CV of 2.4 . Serum adiponectin l
Me PCR conditions for these SYBR-based assays were as described previously [16,17]. Forty rounds of amplification were performed, and fluorescent signals of the Taqman probe or SYBR green signal were used to generate cycle threshold (Ct) values from which mRNA expression levels were calculated. Ct values of HPRT1 and B2M were adjusted to the higher HMBS Ct values. Next, the expression levels of DC