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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
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Inter-quartile after normalization on the reference gene set. cP for Spearman rank correlation test. dP for Mann-Whitney U test. eP for Kruskal-Wallis test, including a Wilcoxon-type test for trend when appropriate. fWith quantitative polymerase chain reaction cut point for positive versus negative ESR1 and PGR, 0.2 and 0.1, respectively, and for ESR2 at the median level of 0.005 (mRNA levels rela
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IcsResultsAssociations of DC-SCRIPT with clinicopathological factors and histological and intrinsic breast cancer subtypesThe relationship between DC-SCRIPT and patient and tumor characteristics was investigated with the use of non-parametric methods (Spearman rank correlations for continuous variables and Wilcoxon rank-sum for dichotomized or Kruskal-Wallis test for ordered variables). To reduce
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Ity Nijmegen Medical Centre, Geert Grooteplein 28, Nijmegen, 6525 GA, The Netherlands Full list of author information is available at the end of the articleof breast cancers. Apart from breast epithelial tumor cells, ESR2 is also expressed in adjacent infiltrating lymphocytes, fibroblasts, and endothelial cells, all of which are known to influence tumor growth [3]. However, its precise role in bre
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Noma in situ; DC-SCRIPT, dendritic cell-specific transcript gene; ERBB2+, HER2neu-positive; ESR, estrogen receptor gene; IDC, infiltrating ductal carcinoma; ILC, infiltrating lobular carcinoma; PGR, progesterone receptor gene; pT1, small tumor without lymphatic/vascular invasion.(Spearman's rho = 0.87; P
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Noma in situ; DC-SCRIPT, dendritic cell-specific transcript gene; ERBB2+, HER2neu-positive; ESR, estrogen receptor gene; IDC, infiltrating ductal carcinoma; ILC, infiltrating lobular carcinoma; PGR, progesterone receptor gene; pT1, small tumor without lymphatic/vascular invasion.(Spearman's rho = 0.87; P
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Ship between DC-SCRIPT mRNA levels measured in primary breast cancers and tumor aggressiveness in a much larger, independent, breast cancer cohort. The main clinical endpoints for assessing the prognostic value of DC-SCRIPT expression were disease-free survival (DFS), metastasis-free survival (MFS), and overall survival (OS) in lymph node-negative (LNN) patients who had not received adjuvant syste
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Receptors also modulate response to therapy [8,9], we also assessed, as a secondary aim of this study, the predictive value of DC-SCRIPT by using clinical benefit and progression-free survival (PFS) after first-line tamoxifen for advanced disease as the main endpoints.Materials and methodsPatientsdetermined by real-time reverse transcriptase-polymerase chain reaction (RT-PCR) [14,16,17]. Follow-up
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Ship between DC-SCRIPT mRNA levels measured in primary breast cancers and tumor aggressiveness in a much larger, independent, breast cancer cohort. The main clinical endpoints for assessing the prognostic value of DC-SCRIPT expression were disease-free survival (DFS), metastasis-free survival (MFS), and overall survival (OS) in lymph node-negative (LNN) patients who had not received adjuvant syste
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Ith DFS, MFS, OS, and PFS, respectively. In multivariable analysis, Cox proportional hazards models for DFS, MFS, OS, and PFS were applied to test DCSCRIPT levels added to models with traditional factors. The proportional hazards assumptions were checked with Schoenfeld residuals. The analyses were stratified if necessary. The models for DFS, MFS, and OS for LNN patients who had not received adjuv