Abstract
Since the late 1990s, infectious agents have been thought to play a role in the pathogenesis of approximately 15% of cancers. It is now widely accepted that infection of stomach tissue with the bacteria Helicobacter pylori is an important cause of stomach adenocarcinoma. In addition, oncogenic viruses, such as papilloma viruses, herpes viruses, and hepadnaviruses are strongly associated with increased risk of cervical cancer, lymphomas, liver cancer, amongst others. However, in the scientific community the percentage of cancers caused by pathogens is believed to be far higher than 15%. A significant volume of data collected to date show an association between infectious agents and urogenital cancers. These agents include Chlamydia trachomatis, Neisseria gonorrhoea, Mycoplasma genitalium and certain viruses that have been implicated in ovarian cancer. Other pathogens include the hepatitis C and Epstein-Barr viruses, which are potentially involved in kidney cancer. In addition, infections with Schistosoma haematobium, the human papillomavirus, and human polyomaviruses are strongly associated with an increased risk of urinary bladder cancer. This article reviews publications available to date on the role of infectious agents in urogenital cancers. A greater understanding of the role of such agents could aid the identification of novel methods of urogenital cancer treatment.
Highlights
Since the late 1990s, infectious agents have been thought to play a role in the pathogenesis of approximately 15% of cancers
Most aggressive ovarian carcinomas arise from ovarian surface epithelium (OSE) cells and account for about 60% of all ovarian carcinomas
Ness and Cottreau [8] suggested that inflammatory-like processes, occurring during ovulation and mediated by gonadotropins, underlie higher cancer risks associated with ovulation and gonadotropin stimulation. This inflammation theory is supported by several epidemiological studies focused on mechanisms that did not affect hormone levels and ovulation, including effects of asbestos and talc exposure, prophylactic hysterectomy and tubal ligation, pelvic inflammatory disease and endometriosis [9,10,11,12,13,14,15,16,17]
Summary
A growing body of evidence indicates that some viruses, bacteria and even helminths might increase cancer risk by promoting general inflammation and subsequently affecting key cellular processes. The exact mechanisms by which the products of how pathogens promote or predispose cells to neoplastic transformation are unknown. One exception is HPV, which has been shown to induce carcinogenesis in cervical epithelial cells by inactivating tumor suppressor proteins. More in-depth and mechanistic studies are required to understand the molecular mechanisms, by which infectious agents could promote carcinogenesis. Such studies could lead to identification of novel methods of urogenital cancer treatment. Competing interests The authors declare that they have no competing interests. Authors’ contributions KA, NK and IB performed literature research and composed the manuscript. All authors read and approved the final manuscript
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