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5, p = 1.1E-15; and DFS, log rank 60.1, p = 4.6E-12), in LN-positive patients (BCSS, log rank 60.9, p = 7.9E-12; and DFS, log rank 4.3, p = 3.0E-8), patients who received no AT (BCSS, log rank 59.7, p = 1.4E-11; and DFS, log rank 47.3, p = 4.9E-9) and those with ER+ tumours who received HT (BCSS, log rank 31.0, p = 9.3E-6; and DFS, log rank 28.5, p = 2.9E-5). To assess the prognostic importance of these phenotypes, a multivariate Cox regression [http://www.selleckchem.com/products/chaetocin.html selleck chemical] model was used to compare their performance to the validated prognostic indicators assessed in the Nottingham/Tenovus whole patient cohort (Table 5) and in patients who had not received any AT subgroup (data not shown). We found that the functional status of p53 transcription pathways remained significantly associated with BCSS, DFS (Table 5) and MFS (data not shown). A similar analysis of the RMH/Breakthrough cohort revealed similar results, for BCSS (p = 0.002), DFS (p = 0.003) and MFS (p = 0.0005). To examine the prognostic significance of the functional status of p53 transcriptional status, the p53 transcription pathway phenotypes were reduced to two groups according to the status of p53 transcriptional activity: (a) active/partially inactive p53 transcription pathway, including p53��/MDM4+/MDM2��/Bcl2��/p21��, p53+/MDM4?/MDM2+/Bcl2+/p21�� and p53��/MDM4?/MDM2?/Bcl2+/p21 �� ; (b) completely inactive p53 transcriptional pathways (two or more inactive p53 [https://en.wikipedia.org/wiki/Tuclazepam tuclazepam] transcriptional pathways), including p53��/MDM4?/MDM2?/Bcl2?/p21?, p53?/MDM4?/MDM2+/Bcl2?/p21?, p53��/MDM4?/MDM2?/Bcl2?/p21+ and p53+/MDM4?/MDM2+/Bcl2?/p21?. In both the Nottingham/Tenovus and the RMH/Breakthrough series, the completely inactive p53 pathways showed a worse clinical outcome (Figure 6). Our exploratory analyses revealed that the functional status of the p53 transcription pathway, ie active/partially inactive versus completely inactive pathway status, was proved to be significant in LN-negative patients (BCSS, log rank 5.4, p = 2.3E-13; and DFS, log rank 36.5, p = 1.5E-9), in LN-positive patients (BCSS, log rank 31.2, p = 2.3E-8; and DFS, log rank 19.2, p = 1.3E-5), patients who received no AT (BCSS, log rank 40.9, p = 1.7E-10; and DFS, log rank 32.7, p = 1.9E-8) and those with ER+ tumours who received HT (p [http://www.selleckchem.com/products/daprodustat.html Angiogenesis inhibitor] p = 1.6E-4). In multivariate Cox regression analysis of the Nottingham/Tenovus series, the completely inactive p53 transcriptional status was an independent predictor of outcome and more powerful than NPI for BCSS [(HR 2.64; 95% CI 1.61�C4.32; p