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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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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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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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Either ESR1-positive and/or ESR2-low pT1 tumors.Introduction Estrogens influence the aggressiveness of breast cancer through their cognate nuclear receptors. In particular, the estrogen receptor-alpha (ERa) (ESR1) - present in tumor cells of about 70 to 75 of all breast tumors is considered crucial because of its proliferationinducing actions and for that reason is an important target for therap
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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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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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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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Uctal carcinoma in situ (DCIS) component or infiltrating lobular carcinoma compared with infiltrating ductal carcinomas (both P
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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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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