OBJECTIVE: To clarify the significance of neuroendocrine differentiation in prostate cancer. METHODS: We immunohistochemically examined 96 samples of prostatic cancers obtained from radical prostatectomies using a specific neuroendocrine marker and various neuropeptides, as well as markers for cell proliferation, angiogenesis and androgen-receptor expression. RESULTS: We frequently found neuroendocrine cells in atrophic glands with or without chronic inflammation in nontumorous tissues. Neuroendocrine cells were detected in 36.5% of prostate cancer samples overall, but had no significant correlation to angiogenesis, cell proliferation or biochemical recurrence. However, patients with a high frequency of neuroendocrine cells (9.4%) tended to undergo preoperative hormonal therapy (p = 0.060), which led to their cancers being atrophic with inflammation. The neuroendocrine cells in these patients contained calcitonin-positive cells (p <or= 0.0001), and calcitonin positivity showed significant association with high Gleason score (p = 0.045) in the group without preoperative therapy. In the group undergoing preoperative therapy, a high prostate-specific antigen titer at first admission correlated to significant biochemical recurrence (p = 0.003). CONCLUSIONS: Neuroendocrine cells may be induced under conditions of atrophy with or without chronic inflammation in both noncancerous glands and in cancers, including calcitonin-positive cells. Neither positive neuroendocrine nor positive androgen-receptor status appears predictive for biochemical recurrence. Copyright 2009 S. Karger AG, Basel.
OBJECTIVE: To clarify the significance of neuroendocrine differentiation in prostate cancer. METHODS: We immunohistochemically examined 96 samples of prostatic cancers obtained from radical prostatectomies using a specific neuroendocrine marker and various neuropeptides, as well as markers for cell proliferation, angiogenesis and androgen-receptor expression. RESULTS: We frequently found neuroendocrine cells in atrophic glands with or without chronic inflammation in nontumorous tissues. Neuroendocrine cells were detected in 36.5% of prostate cancer samples overall, but had no significant correlation to angiogenesis, cell proliferation or biochemical recurrence. However, patients with a high frequency of neuroendocrine cells (9.4%) tended to undergo preoperative hormonal therapy (p = 0.060), which led to their cancers being atrophic with inflammation. The neuroendocrine cells in these patients contained calcitonin-positive cells (p <or= 0.0001), and calcitonin positivity showed significant association with high Gleason score (p = 0.045) in the group without preoperative therapy. In the group undergoing preoperative therapy, a high prostate-specific antigen titer at first admission correlated to significant biochemical recurrence (p = 0.003). CONCLUSIONS: Neuroendocrine cells may be induced under conditions of atrophy with or without chronic inflammation in both noncancerous glands and in cancers, including calcitonin-positive cells. Neither positive neuroendocrine nor positive androgen-receptor status appears predictive for biochemical recurrence. Copyright 2009 S. Karger AG, Basel.
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