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A 61-year-old man presented to the oncology clinic with Gleason 9 (4 + 5) prostate cancer. Staging CT showed multiple nodules in both lungs. Since the lung lesions were too small for biopsy, he was started on anti-androgen therapy for suspected metastatic, hormone-sensitive prostate cancer. While his prostate-specific antigen decreased from 32 to <0.1 ng/ml, the multiple lung lesions showed no response on subsequent imaging. The patient presented during follow-up with severe right leg pain, at which time magnetic resonance imaging revealed a large, hyperintense mass in the femur. The mass was resected along with two lung nodules, with pathology demonstrating metastatic alveolar soft part sarcoma. This serves as an important reminder that lesions suspicious for metastases may be due to cancers of multiple primary origins, particularly if the pattern of metastasis is atypical or there is varied response to therapy. [ABSTRACT FROM AUTHOR]

Although cancer of the prostate (CaP) is the most commonly occurring cancer in males, there are major limitations in its diagnosis and long-term cure. Consequently, understanding the molecular mechanisms involved in the progression of CaP is of particular importance for production of pharmacological and biological agents to manage the disease. The development of the normal prostate is regulated by stromal–epithelial interactions via endocrine and paracrine factors, such as androgens and growth factors, which act as precise homeostatic regulators of cellular proliferation. Importantly, after a period of hormonal therapy, CaP shifts from an androgen-dependent to an androgen-independent state with a concomitant switch from paracrine to autocrine growth factor stimulation and subsequent upregulation of growth factor expression. Thus, growth factors and their receptors have a pivotal role in CaP. This is emphasized by current evidence obtained from clinical specimens as well as several in vitro and in vivo models strongly suggesting that epidermal growth factor and the neurotrophins (nerve growth factor, brain derived neurotrophin factor, neurotrophin-3 and neurotrophin-4/5) together with their tyrosine kinase receptors could play a very significant role in CaP progression. [Copyright &y& Elsevier]