Objective To determine the value of serum chromogranin A (CgA), a marker of neuroendocrine differentiation, for monitoring prostate cancer; CgA levels were related to three other tumour markers, i.e. total prostate‐specific antigen (tPSA), prostatic acid phosphatase (PAP), neurone‐specific enolase (NSE), and to testosterone, to assess the importance of hormone withdrawal. Patients and methods Serum samples (218) were obtained from 118 patients with prostate cancer, including 111 patients with advanced prostate cancer; 103 presented to our centre for systemic radionuclide therapy of painful skeletal metastases. CgA concentrations were measured using a new immunoradiometric assay (IRMA; Cis Bio International, Gif sur Yvette, France) and a threshold of 70 ng/mL was determined after receiver operating characteristic curve analysis. Testosterone was also measured with an IRMA assay; tPSA, PAP and NSE were assayed using the time‐resolved amplified cryptate emission. Results Serum marker levels were high in 64% of the patients for CgA, 24% for NSE, 89% for tPSA and 81% for PAP. Patients resistant to endocrine treatments and with elevated tPSA (i.e. hormone‐independent) showed increased CgA and NSE in 62% and 29%, respectively. Patients with hormone‐dependent prostate cancer (i.e. with a normal tPSA level) had elevated CgA in 59% but no abnormal NSE. All patients of the latter group except one showed clinical progression of their disease. However, the mean (sd) concentrations of CgA in hormone‐independent (146) or hormone‐dependent (22) patients, at 185.3 (449.1) and 160.9 (293.9) ng/mL, respectively, were not statistically different (P = 0.8, Mann–Whitney U‐test). For 30 patients, blood samples were drawn and markers measured before and after systemic radionuclide therapy. There was a significant increase in the CgA and tPSA concentrations after treatment (P = 0.0146 and 0.0025, respectively). Conclusions In association with tPSA, serum CgA appears to be a promising marker for monitoring patients with prostate cancer.

Type II gene expression can be detected using FBT11-II. This specific recognition could improve the clinical usefulness of assays aimed at either managing aggressive tumors or screening for Down syndrome.

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