[Osteosarcoma of the prostate after radiotherapy]. / Osteosarkom der Prostata nach Strahlentherapie.

Osteosarcoma of the prostate is a rare finding. These tumours usually occur years after radiotherapy for prostate cancer. We report the case of a 74-year-old man with prostate cancer who had been treated with radiotherapy and androgen deprivation therapy. The man presented with urinary retention and his prostate was transurethrally resected. The histopathological investigation showed formations of a poorly differentiated osteosarcoma in the prostate. Because of serious comorbidities we decided to withhold chemotherapy considering its potential side effects. The man died a few months after the diagnosis of osteosarcoma in the prostate with the disease in a metastatic stage. In conclusion, osteosarcoma of the prostate is a rarely reported consequence of radiotherapy in patients with prostate cancer and is characterised by poor life expectancy.

Biomarkers for early prostate cancer detection.

In the 1990s the discovery of prostate-specific antigen (PSA) revolutionized early prostate cancer detection. Since that time, PSA has become an indispensable marker for diagnosis and follow up of prostate cancer patients. Despite its remarkable performance, PSA is not cancer specific. High PSA levels are found in both cancerous and healthy tissue, particularly in benign prostate disease, resulting in significant numbers of false positive cases. Hence, there is a need for new markers that better differentiate benign from malignant lesions and indolent from aggressive cancers to decrease the potential over treatment of prostate cancer. With recent advances in biotechnology, many promising blood biomarkers have been identified and are currently under investigation. This article reviewed the literature searching for emerging biomarkers for early prostate cancer detection.

Antagonists of growth hormone-releasing hormone (GH-RH) enhance tumour growth inhibition induced by androgen deprivation in human MDA-Pca-2b prostate cancers.

In the present study, we investigated whether the growth hormone-releasing hormone (GH-RH) antagonist JV-1-38 could enhance the effects of androgen deprivation produced by the anti-androgen Flutamide and luteinising hormone-releasing hormone (LH-RH) agonist Decapeptyl in an experimental model of human androgen-sensitive MDA PCa 2b prostate carcinoma implanted subcutaneously (s.c.) into nude mice. We also evaluated by reverse transcriptase-polymerase chain reaction (RT-PCR) the effects of combined treatment on the mRNA expression for prostate-specific antigen (PSA) and measured serum PSA levels. In experiment 1, GH-RH antagonist JV-1-38 greatly inhibited tumour growth in combination with Decapeptyl, but was ineffective when given alone. Thus, combined therapy with JV-1-38 at 20 microg/day and Decapeptyl microcapsules releasing 12.5 microg/day for 29 days inhibited significantly (P<0.01) MDA PCa 2b tumour growth by 65%, compared with controls. Combined treatment also significantly (P<0.05) decreased serum PSA levels by 52% and reduced tumour weight by 54% vs. controls. In experiment 2, GH-RH antagonist JV-1-38 at 20 microg/day likewise showed powerful growth inhibitory effects when combined with Flutamide (25 mg/kg/day) for 21 days. Combined treatment with JV-1-38 and slow-release pellets of Flutamide significantly (P<0.001) inhibited tumour growth by 61% versus controls, and was significantly (P<0.05) more effective than Flutamide or JV-1-38 alone. Combination therapy also reduced significantly (P<0.001) tumour weight and serum PSA levels by 59 and 47%, respectively. The mRNA expression for PSA in MDA PCa 2b tumours was not changed by JV-1-38, Decapeptyl and Flutamide alone or in their respective combinations. Our findings suggest that GH-RH antagonists could enhance the tumour inhibitory effects of androgen deprivation for the primary therapy of patients with advanced prostate carcinoma.