Decipher messenger export
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Decipher messenger export trial#
First, the study has a smaller sample size due to the availability of specimens and represents a subset of the trial cohort, although we observed a clear treatment effect in the analytic cohort which was consistent with the overall cohort.
Decipher messenger export plus#
Nonetheless, an initial report from the randomized phase III TITAN trial in mHSPC of ADT versus ADT plus apalutamide (an AR inhibitor shown to improve OS in this setting) demonstrated a greater benefit in radiographic progression-free survival from combination therapy in basal, compared with luminal subtype.
Decipher messenger export Pc#
Preclinical drug response models suggest that luminal B PC is associated with increased taxane sensitivity versus basal subtype however, the reasons for this remain unclear. Second, unique biological features of luminal B versus basal mHSPC may govern response to docetaxel. First, and more simplistically, poor-prognostic disease profiles may preferentially benefit from early treatment intensification with docetaxel as reflected by the greater magnitude of benefit from chemohormonal therapy seen in patients with de novo high-volume presentation and the GC Q4 (highest) subgroup. The observation that luminal B subtype (and not basal subtype) retained OS benefit from docetaxel may have two possible explanations.
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Clinical outcomes of patients by AR activity (AR-A) This can be represented as an absolute benefit in OS for addition of docetaxel to ADT for men with tumors in GC Q1 versus GC Q4 of 9% versus 25% at 3 years, respectively ( Supplementary Figure S5, available at ). The effect of docetaxel on OS was observed across all GC groups however, the relative benefit of chemohormonal therapy varied by GC group was significant with higher GC (higher risk) disease (Q1: HR 0.72, 95% CI 0.29-1.73 Q2-3: HR 0.57, 95% CI 0.30-1.05 and Q4: HR 0.41, 95% CI 0.19-0.84 Figure 4A). Similar results were seen when GC was analyzed categorically (not shown). In the overall cohort, GC significantly stratified both ttCRPC and OS, with Q1, Q2-3, and Q4 cut-off subgroups showing 3-year OS rates of 77%, 60%, and 31%, respectively ( Supplementary Figure S2B, available at ). No differential treatment benefit by subtype was observed with respect to ttCRPC ( Figure 4B and Supplementary Figures S3A and S4A, available at ). No substantial differences in receipt of OS-improving therapies upon disease progression were noted when comparing luminal B and basal subtypes ( Supplementary Table S4, available at ). In the luminal B subgroup, there was an improvement in OS with docetaxel (median OS: 29.8 versus 52.1 months HR 0.45, 95% CI 0.25-0.81 P = 0.007), suggesting a potential treatment–biomarker interaction. Patients with basal disease showed no evidence of a significant OS benefit from docetaxel (median OS: 47.1 versus 49.2 months HR 0.85, 95% CI 0.47-1.54 P = 0.584 Figures 3 and 4A ), even in the subgroup of patient with high-volume disease. We then tested the OS benefit associated with the addition of docetaxel split by transcriptomic subtype.
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Luminal B subtype was associated with poorer OS on ADT alone versus basal subtype (median OS: 29.8 versus 47.1 months HR 1.75, 95% CI 0.99-3.10 P = 0.052 Figure 2A). Table 1 Multivariable analysis of OS and time to CRPC.