Inflammation Oxidative Stress and Preneoplasia in a Mouse Model of Chronic Bacterial Prostatitis
Abstract
Prostate cancer (PCA) is the most common cancer in men and, second to lung cancer, causes the greatest number of deaths in American males (1,2). While the exact etiology of PCA is largely unknown, it is a multifactorial disease in which several environmental and genetic factors are likely involved (3,4). Epidemiological studies have shown that environmental factors and lifestyle contribute to the development of the disease (5). North Americans and Northern Europeans have the high rates of disease while men in Asian nations experience lower rates (2). Risk is also strongly associated with a family history of the disease, and several susceptibility genes or loci are currently under investigation (6,7). Other etiological factors such as androgens (8), growth factors (9), diet (10-16), sexually transmitted diseases (17), and infection with other infectious agents (18) may contribute to increased susceptibility. Over the past several decades, a number of epidemiological studies have identified an association between specific bacterial infections and PCA (18). A recent meta-analysis of fl%the literature has demonstrated an increased risk for PCA in men with a history of prostatitis (19). Other investigations of infectious agents in the etiology of chronic prostatitis/chronic pelvic pain syndrome have shown a correlation between the presence of bacterial genes and inflammation in prostate biopsy specimens (20). Chronic or recurrent prostatic inflammation, known to inflict cellular oxidative damage, may thus contribute to the development of PCA.
Document Details
- Document Type
- Technical Report
- Publication Date
- Sep 01, 2005
- Accession Number
- ADA447404
Entities
People
- Walter J. Hopkins
Organizations
- University of Wisconsin–Madison