Cristina Magi Galluzzi and Angelo M De Marzo Introduction

Prostate cancer (PCA) is the most common non-skin malignancy diagnosed in men in the USA and the second leading cause of cancer deaths among North American and Western European men. The incidence of PCA and the rate of death due to the disease increase with age. Less than 1% cases of PCA are diagnosed under the age of40, although small PCAs have been detected in up to 29% men 30 to 40 years of age in autopsy series (1). The incidence and mortality rates are highest among African American men, being 2.0-fold higher than in Caucasian Americans, whereas lower rates are characteristic of the Asian population (2).

Etiologic factors associated with PCA are varied and comprise both genetic and environmental influences. Among the genetic factors aging, family clustering, race, and hormonal influences seem to play a major role. A diet high in animal fat and red meat and poor in fruits and vegetables, and the preventive use of antioxidants associated with a high intake oftomatoes are also critical factors (3,4).

Accumulating data suggests that normal and neoplastic prostate cells may be subjected to multiple genome-damaging stresses, and that both diet and male sex steroids may modulate the level of threatening insults. A model of carcinogenesis and progression similar to colon cancer has been proposed for PCA (Figure 1) (5). This model predicts multiple steps in the process from normal prostatic epithelium to invasive cancer through the intermediate step ofprostatic intraepithelial neoplasia (PIN) and/or proliferating intermediate luminal cells. The most important feature of such a model is the gradual accumulation of changes in critical genes rather than their order of occurrence.

PIN, in particular the high-grade form, has been extensively studied and considered as the major morphological identifiable putative precursor of PCA (6, 7). However, it is likely that PCA might also arise from precursor lesions other than PIN, some not yet identifiable with certainty at the present time. PCA develops in two different regions of the gland, with the majority of the lesions (approximately 80%) found in the peripheral zone (PZ), and most of the remaining cancers in the region surround the peri-urethral region, termed the transition zone (TZ).

Inflammation, dietary factors, inherited factors

Figure 1. The molecular pathogenesis of prostate cancer.

Inflammation, dietary factors, inherited factors

Figure 1. The molecular pathogenesis of prostate cancer.

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