Kasey Kissick
Prostate cancer is a common diagnosis. In fact, it is the most common non-cutaneous malignancy diagnosed and the second leading cause of cancer death in men in the United States.1 Due to increasing life expectancies, this late-onset cancer has seen a marked increase in incidence over the last few decades. Despite its widespread and growing prevalence, little is understood about the actual causes of prostate cancer. The only known risk factors are family history, age, and race. Although African Americans have the highest rates of prostate cancer, the reason for this prevalence is unknown.1 Even more perplexing is the fact that that men living in Asia are much less likely to develop prostate cancer than those in the US or Western Europe. However, when Asian men move to western countries, their risk increases.2 These results indicate that prostate cancer risk is not simply the result of genetics and aging. Like many other cancers, environmental factors may be involved. Current prostate cancer research is investigating the role of dietary factors, chemical agents, cigarette smoke, and infectious agents like bacteria and viruses.
Most would be surprised to learn that a number of cancers have infectious origin, but the American Cancer Society reports that 20% of all cancers are triggered by infections. To name a few pairs: Hepatitis B virus and liver cancer, human papillomavirus (HPV) and cervical cancer, schistosomes and bladder cancer, and the ulcer-causing bacteria, Helicobacter pylori, and stomach cancer. Some microbes induce carcinogenesis by directly targeting and damaging DNA, like HPV does with cervical cancer. Others, like H. pylori in stomach cancer, trigger a chronic inflammatory immune response, which damages DNA over time.3 In many cases, discovering the infectious agents involved in cancers can be difficult because the cancer develops years or even decades after infection. Establishing these links requires time-intensive, large-scale epidemiological studies to select and confirm suspected infection candidates. H. pylori, for instance, was linked to stomach ulcers in 1980, but it took 10 years, 12 studies, and a grand total of 1128 cases and 3406 controls to confirm that infection with the bacteria was associated with an increased risk of stomach cancer.4
Although it can take many years to confirm a suspected relationship, uncovering a link between an infectious agent and cancer is of immense public health importance. Identification of the potential cause and effect facilitates preventive measures and early treatment. In the case of HPV and cervical cancer, the Gardasil vaccine is estimated to protect against 70% of cervical cancers.5 Likewise, the discovery that H. pylori increases stomach cancer risk 6-fold could be crucial to preventing stomach cancer by screening for and treating ulcers early with antibiotics.4 Similarly, schistosomes can be screened and treated with a round of anti-helminthic drugs to eliminate the parasite before the onset of bladder cancer. Knowing that a certain virus or bacteria may predict cancer later in life completely changes the picture; with such knowledge, cancer prevention becomes a very attainable goal. Dr. Jonathan Simons, president and CEO of the Prostate Cancer Foundation explains, “discovering the pathogens that cause cancer has been transformational in reducing death and suffering and in generating entirely new prevention strategies.” The potential to significantly cut healthcare costs, save lives, and alleviate suffering is what makes this preventive research so worthwhile.
In the case of prostate cancer, many signs suggest an infectious agent may play a role in its pathogenesis. Mirroring the relationship between H. pylori and stomach cancer, an infection causing chronic inflammation may, over time, lead to prostate cancer. Several bacteria, viruses, and parasites have been observed to infect the prostate and generate an inflammatory response, and studies show that regular users of anti-inflammatory agents such as aspirin report a reduced risk of developing prostate cancer.1 Current evidence suggests that some unidentified infection occurs early in life and produces chronic, asymptomatic inflammation in the prostate, which after 20-30 years, leads to prostate cancer.1 Two microorganisms at the top of suspect list include the protozoan parasite, Trichomonas vaginalis, and the notoriously widespread and asymptomatic bacterial family of Mycoplasma.6,7 Both produce chronic, largely unrecognized infections. Interestingly, both infections are more prevalent in African Americans, perhaps explaining the mystery of race as a risk factor.6,7
Currently, no conclusive data exists revealing a strong association between a single microbe and prostate cancer. The time lag and symptomless nature of many prostate infections make confirming the role of an infectious agent a challenge. Additionally, research of the prostate is limited, and there is still much uncertainty about what constitutes the normal bacterial flora of the prostate. With this knowledge, it would be easier to pinpoint the agents that might be producing an inflammatory, cancerous effect.
Solidifying the link between an infectious agent and prostate cancer may not, however, be the sole answer. There could be multiple microbes involved or a number of cofactors, such as dietary issues, that could interact to create the conditions necessary for prostate cancer. Despite the challenges, researchers remain optimistic. Simons calls this search “one of the highest public health issues of our era.” Moving forward, he believes “the obvious suspects are usually never responsible, and it will require innovation and discovery with new biotechnologies and insights from innovative young scientists to elucidate the microbe or microbes that are responsible.” With modern diagnostic technologies and growing interest in research on cancer and infection, a discovery may occur soon.
Jonathan Simons, president and CEO of the Prostate Cancer Foundation, is a recognized physician-scientist and leader in prostate cancer research. Simons attended Johns Hopkins Medical School where he completed a clinical fellowship in medical oncology and a post-doctoral fellowship in human cancer molecular genetics.
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