Review
Infection, inflammation and prostate carcinogenesis

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Abstract

Several reports have shown that the incidence of prostate cancer is on the increase and that more men would be diagnosed of prostate cancer in the next decades. Many approaches are being applied towards reducing the cases of prostate cancer, especially in the very rich countries. However, these have not been effective due to the poor current understanding of the pathophysiology of prostate carcinogenesis. The current work presents a review of how chronic infection and inflammation may contribute to prostate carcinogenesis.

Introduction

Current data indicates that the prevalence of prostate cancer across the Western World is increasing at an alarming rate. Recent studies have shown that prostate cancer is the most common form of cancer in men in the United State of America, and the second leading cause of death due to cancer [1]. Approximately 100 men are being diagnosed with this disease daily in the United Kingdom [2]. There are many factors that contribute to the development of prostate cancer, the most important of them are age, family history, diet [3]. For instance, men at older age are commonly diagnosed with advanced disease whereas the early form of the disease is seen at younger age often at 50 [3].

The risk of developing prostate cancer varies across many geographic populations; 16.6%, 18.1%, and 1 in 100,000 chance of developing prostate cancer have been reported [4]. Studies show that people from low risk geographic populations such as the Chinese and Japanese, who changed their residence to a place in the Western Nations, had an increased chance of developing prostate cancer [5]. Though some authors have argued that the increase in prostate cancer risk among people who immigrated to the west; might be that the people already had the latent form of prostate tumour before they relocated [6], there are evidences suggesting that up to 30% of men in the general population aged from 50 years and above, irrespective of geographic origin have foci of prostate neoplastic growth [5], [6].

There are many researchers across different research Institutions whose works have been focused on preventive measures for prostate cancer. In this regard, some measures such as dietary approaches have been suggested [3], [7], [8]. Though conflicting reports exist for intake of certain dietary supplements like Selenium and vitamin E and dietary fat [9], [10], there is a consensus across recent studies that dietary in takes including lycopene from tomatoes, vitamin E, and Selenium may protect from prostate cancer [7], [8], [11]. This approach has not been effective due to our poor understanding of several contributing factors for prostate carcinogenesis. Emerging reports now demonstrate that local infections affecting the prostate may elicit changes that may support carcinogenesis by first inducing chronic local inflammation and other immunogenic responses. The aim of the current study is to review the role of factors which can induce local inflammation of the prostate including infectious agents and prostate carcinogenesis.

Section snippets

Anatomy and physiology of prostate gland

The human prostate is a gland of the male reproductive system that produces fluid which helps semen to transport sperm during male orgasm. Prostate is a small-about the same size and shape as walnut, located in front of the rectum and just below the bladder; and wraps the urethra round. The mammalian prostate gland is made up of three important zones. Two of which are prone to specific prostate diseases; for example, while benign prostatic hyperplasia arises in the transitional zone; most

Inflammation and prostate cancer

Current evidences suggest that inflammation may contribute to carcinogenesis of prostate cancer. This was shown by both epidemiological and histopathological studies. It was estimated that one fifth of prostate cancer cases were as a result of chronic inflammation due to infectious agents and or environmental factors [15]. The term proliferative inflammatory atrophy (PIA) was first used by De Marzo and colleagues [16] in 1999 to describe prostatic lesions with increased inflammatory cells. The

Experimental evidence

Using an animal model, Elkahwaji and his colleagues [17] investigated the link between infection-induced chronic inflammation of the prostate and the changes in prostate epithelium. They inoculated the prostate of mice with gram negative bacterial and observed acute inflammation after 5 days and chronic inflammation after 12 weeks of the inoculation. From histologic evidence, the group found atypical hyperplasia, dysplasia and increased prostatic epithelial proliferation in the prostate of the

Clinical evidences

In epidemiological study, Dennis et al. [18] pooled published papers since 2002 and conducted a meta analysis and examined the relationship between chronic inflammation of the prostate and prostate cancer. They author found an increased risk of prostate cancer among men with history of Prostatis or chronic inflammation of the prostate (odd ratio 1.6) and an increased relative risk for prostate cancer in men who had syphilis and gonorrhoea infection. Also, evidence from study which performed the

Pathophysiology of inflammatory basis of prostate cancer

Inflammation has been associated with about 20% of cancers in human [15] by causing genomic damage [20], [21]. Some environmental factors including infectious agents for instance, bacteria and virus have been implicated for inducing prostatic inflammation and prostate cancer. Other factors such as dietary habits, physical trauma, hormone imbalance, and metabolic products such as uric acid have been associated with prostatic inflammation [20], [22], [23], [24].

Molecular mechanism of oxidation induced prostate cancer

The molecular mechanisms responsible for inflammation mediated prostate cancer are not yet clear. However, there are indications that this form of cancer transformation may not be soley due to infectious agents their selves, but rather, may be as a result of the presence of pathogen encoded oncogenes [15]. Emerging evidences suggest that both innate and adaptive immune response may have huge contributions during inflammation – induced prostate cancer transformation [15], [20], [38], [39]. The

Conflict of interest statement

None declared.

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