Abstract

Abstract Background &Aims: Curcumin, a polyphenol derived from Curcuma Longa is known for his anti-cancer activity and may exert synergic effects with cytotoxic agents. In parallel, neuroendocrine differentiation in castration-resistant prostate cancer provides an aggressive phenotype to disease. In this prospective phase II study, we assessed the impact of a new combination, docetaxel plus curcumin, in patients with or without neuroendocrine features. Methods: In this phase II study, thirty patients received docetaxel 75 mg/m*2 (perfusion given every 3 weeks) in combination with curcumin orally at 6 g/day (day-4 to day+2 of docetaxel). Neuroendocrine features were determined by serum chromogranin A and neuron-specific enolase, before each cycle. Variations were divided in 3 groups: an increase > 25%, a decrease of 50% or greater and stability. Treatment response were measured by PSA >50% decrease (PSA response) and objective response rate on evaluable metastatic lesions. Results: Initially, 53% of patients had an elevated chromogranin A and 33% an elevated neuron-specific enolase. During treatment, 7% performed a > 50% chromogranin A decrease and 30% a neuron-specific enolase decrease. PSA response was observed in 59% of patients and 40% out of patients with evaluable targets had a partial response. PSA and objective response rate were identical whatever neuroendocrine feature. A positive correlation was found between chromogranin A and PSA, age, weight and palliative radiotherapy. Conversely, neuron-specific enolase was negatively correlated with PSA and patients'age. Conclusions: Curcumin and docetaxel had a global action on tumors with or without neuroendocrine features. Chromogranin A was the best neuroendocrine marker in correlation with clinical parameters. This association delivered then remarkable results on neuroendocrine differentiation of castration-resistant prostate cancer, in comparison with pivotal study data with docetaxel alone (TAX 327). Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 2694. doi:1538-7445.AM2012-2694

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