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A Berruti
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A Mosca
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M Tucci
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C Terrone
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M Torta
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R Tarabuzzi
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L Russo
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E Bollito
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R M Scarpa
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A Angeli
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L Dogliotti
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The presence of neuroendocrine (NE) differentiation in the context of predominantly exocrine prostate cancer may play a key role in androgen-independent tumor growth. The prognostic significance of plasma chromogranin A (CgA) was assessed in a series of consecutive prostate cancer patients with hormone-refractory disease.

One hundred and eight patients with newly diagnosed hormone-refractory prostate cancer entered the study. Plasma CgA levels and other biochemical parameters, such as serum prostate specific antigen, serum alkaline phosphatase, serum lactate dehydrogenase, serum albumin and hemoglobin concentration, were measured at baseline (i.e. when hormone refractoriness occurred) and their prognostic role was evaluated together with patient performance status, Gleason score (at diagnosis of prostate cancer) and the presence of visceral metastases. Furthermore, plasma CgA was prospectively evaluated in 50 patients undergoing chemotherapy.

At baseline, 45 patients (43.3%) showed elevated CgA values. Plasma CgA negatively correlated with survival, either in univariate analysis (P=0.008) or in multivariate analysis, after adjusting for previously mentioned prognostic parameters (P<0.05). In the patient subset undergoing chemotherapy, median CgA (range) values were 13.3 (3.0–141.0) U/l at baseline, 19.1 (3.0–486.0) U/l after 3 months, 20.8 (3.0–702.0) U/l after 6 months and 39.4 (3.0–414.0) U/l after 9 months (P<0.01). The corresponding supranormal rates were 17/50 (34%), 23/50 (46%), 26/50 (52%) and 34/50 (68%) respectively (P<0.005).

Elevated plasma CgA levels are frequently observed in prostate cancer patients with hormone-refractory disease and correlate with poor prognosis. NE differentiation in hormone-refractory patients is a time-dependent phenomenon and is not influenced by conventional antineoplastic treatments.

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A Bottini Breast Unit and Anatomia Patologica Azienda Ospedaliera Istituti Ospitalieri, Cremona, Dipartimento di Scienze Cliniche e Biologiche, Universitàdi Torino, Oncologia Medica, Azienda Ospedaliera San Luigi, Orbassano, Italy

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A Berruti Breast Unit and Anatomia Patologica Azienda Ospedaliera Istituti Ospitalieri, Cremona, Dipartimento di Scienze Cliniche e Biologiche, Universitàdi Torino, Oncologia Medica, Azienda Ospedaliera San Luigi, Orbassano, Italy

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M P Brizzi Breast Unit and Anatomia Patologica Azienda Ospedaliera Istituti Ospitalieri, Cremona, Dipartimento di Scienze Cliniche e Biologiche, Universitàdi Torino, Oncologia Medica, Azienda Ospedaliera San Luigi, Orbassano, Italy

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A Bersiga Breast Unit and Anatomia Patologica Azienda Ospedaliera Istituti Ospitalieri, Cremona, Dipartimento di Scienze Cliniche e Biologiche, Universitàdi Torino, Oncologia Medica, Azienda Ospedaliera San Luigi, Orbassano, Italy

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D Generali Breast Unit and Anatomia Patologica Azienda Ospedaliera Istituti Ospitalieri, Cremona, Dipartimento di Scienze Cliniche e Biologiche, Universitàdi Torino, Oncologia Medica, Azienda Ospedaliera San Luigi, Orbassano, Italy

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G Allevi Breast Unit and Anatomia Patologica Azienda Ospedaliera Istituti Ospitalieri, Cremona, Dipartimento di Scienze Cliniche e Biologiche, Universitàdi Torino, Oncologia Medica, Azienda Ospedaliera San Luigi, Orbassano, Italy

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S Aguggini Breast Unit and Anatomia Patologica Azienda Ospedaliera Istituti Ospitalieri, Cremona, Dipartimento di Scienze Cliniche e Biologiche, Universitàdi Torino, Oncologia Medica, Azienda Ospedaliera San Luigi, Orbassano, Italy

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G Bolsi Breast Unit and Anatomia Patologica Azienda Ospedaliera Istituti Ospitalieri, Cremona, Dipartimento di Scienze Cliniche e Biologiche, Universitàdi Torino, Oncologia Medica, Azienda Ospedaliera San Luigi, Orbassano, Italy

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S Bonardi Breast Unit and Anatomia Patologica Azienda Ospedaliera Istituti Ospitalieri, Cremona, Dipartimento di Scienze Cliniche e Biologiche, Universitàdi Torino, Oncologia Medica, Azienda Ospedaliera San Luigi, Orbassano, Italy

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B Tondelli Breast Unit and Anatomia Patologica Azienda Ospedaliera Istituti Ospitalieri, Cremona, Dipartimento di Scienze Cliniche e Biologiche, Universitàdi Torino, Oncologia Medica, Azienda Ospedaliera San Luigi, Orbassano, Italy

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F Vana Breast Unit and Anatomia Patologica Azienda Ospedaliera Istituti Ospitalieri, Cremona, Dipartimento di Scienze Cliniche e Biologiche, Universitàdi Torino, Oncologia Medica, Azienda Ospedaliera San Luigi, Orbassano, Italy

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M Tampellini Breast Unit and Anatomia Patologica Azienda Ospedaliera Istituti Ospitalieri, Cremona, Dipartimento di Scienze Cliniche e Biologiche, Universitàdi Torino, Oncologia Medica, Azienda Ospedaliera San Luigi, Orbassano, Italy

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P Alquati Breast Unit and Anatomia Patologica Azienda Ospedaliera Istituti Ospitalieri, Cremona, Dipartimento di Scienze Cliniche e Biologiche, Universitàdi Torino, Oncologia Medica, Azienda Ospedaliera San Luigi, Orbassano, Italy

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L Dogliotti Breast Unit and Anatomia Patologica Azienda Ospedaliera Istituti Ospitalieri, Cremona, Dipartimento di Scienze Cliniche e Biologiche, Universitàdi Torino, Oncologia Medica, Azienda Ospedaliera San Luigi, Orbassano, Italy

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This study was designed to address whether simultaneous primary chemo-hormonal therapy provides additional activity compared with chemotherapy alone in breast cancer patients with operable or locally advanced disease. Between January 1997 and January 2002, 211 consecutive patients with T2–4, N0–1, M0 breast cancer were randomized to receive either epirubicin alone (EPI) or epirubicin plus tamoxifen (EPI-TAM). Ki67 expression was evaluated immunohistochemically in tumor specimens obtained before chemotherapy by incision biopsy and at definitive surgery. Tumor shrinkage of >50% was obtained in 76% of patients randomized in the EPI arm and 81.9% of patients randomized in the EPI-TAM arm (not significant). The corresponding rates of clinical and pathological complete response were 20.2 and 21.9% (not significant), and 4.8 and 6.7% (not significant), respectively. Pathologically complete response was more frequently observed in estrogen receptor (ER)-negative (ER−) tumors (P=0.04) and correlated with elevated baseline Ki67 expression (P<0.01). Both EPI and EPI-TAM treatments resulted in a significant reduction in Ki67 expression, either in overall patients (P=0.000) or in patients with ER+ breast cancer (P=0.000). The reduction in Ki67 immunostaining in the EPI-TAM arm was greater than in the EPI arm, leading to a lower Ki67 expression at post-operative residual histology (P=0.0041). The addition of tamoxifen to epirubicin chemotherapy did not improve the response rate but led to a significantly higher reduction in the Ki67 expression. Baseline elevated Ki67 expression and the ER− status were both associated with a greater chance of obtaining a pathological complete response at residual histology.

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