Epidemiological and clinical features
Prostate cancer is the most common male malignancy and the second most common cause of cancer-related death in many Western industrialized countries. In Finland, the age-adjusted incidence rate was 85.6 per 100 000 men in 2011 (totaling 4719 new cases), and the mortality rate was 13.5 per 100 000 men (886 deaths) according to Finnish Cancer Registry.
A special feature of prostate cancer is that a latent form of the disease is very common. Microscopic lesions of cancer have been found in autopsies from more than 50% of 70-80 year old men. A vast majority of these histological cancers would most probably never develop to a clinical cancer. Whether these incidentally found small carcinomas represent the same disease entity as the clinically relevant, life-threatening tumors, is not really known.
Prostate cancer arises from the glandular epithelium, most often in the peripheral zone of the prostate. Prostate cancer progression is a multistep process, in which an organ-confined tumor eventually invades through the capsule of the prostate into its surroundings and metastasizes to local lymph nodes and to distant organs, mainly bones. The effect of prostate cancer cells on bone appears to be mainly osteoblastic, leading to bone destruction and pain, and other complications including pathological fractures. At the end-stage of the disease, prostate cancer metastasizes throughout the body.
|Figure. Multi-step progression of prostate cancer. The cancer arises from normal epithelial cells, at least in some cases through premalignant lesions called proliferative inflammatory atrophy (PIA) or prostate intraepithelial neoplasia (PIN). The common latent microscopic prostate cancers may also be pre-stages of clinical cancer. However, the potential of the latent cancer to progress into a theoretically life-threatening clinical cancer is not known. Prostate cancer metastasizes, in the first place, mainly to local lymph nodes and bone. The growth of the vast majority of prostate cancers is androgen-dependent. However, during androgen withdrawal treatment, a castration-resistant tumor clone eventually emerges. Majority of these castration-resistant tumors are still androgen-sensitive.|