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Prostate cancer is the second most common nondermatologic cancer in males in the United States. The median age at diagnosis is 66 years and median age at death is 80 years, with most patients diagnosed between ages 55 and 74 years. Black men are at greatest risk of developing and dying of prostate cancer. The U.S. Preventive Services Task Force (USPSTF) and American Urological Association (AUA) guidelines recommend shared decision-making in consideration of screening for men ages 55 to 69 years. Currently, digital rectal examination alone is not recommended for prostate cancer screening. The serum prostate-specific antigen (PSA) test remains the most common screening tool. Novel formulas and algorithms, including the Prostate Health Index (phi) and the 4Kscore, which use total PSA, free PSA, and other information to estimate risk, have shown greater predictive values for detection than the PSA test. Risk assessment with magnetic resonance imaging (MRI) study with or without MRI/transrectal ultrasonography (TRUS) targeted biopsy requires fewer biopsy specimens than traditional TRUS-guided biopsy, and is associated with higher detection rates. Studies of specific lifestyle modifications to minimize prostate cancer risk have shown inconclusive results; however, high carbohydrate and animal fat intakes may increase the risk.

Case 1. Darrell is a 59-year-old Black man with a history of obesity and hypertension. He comes to your office today for an annual health maintenance examination. He has no family history of genitourinary cancers and no lower urinary tract symptoms. During the history and physical examination, he does not ask about cancer screening, so you initiate a discussion about prostate cancer screening.

Pathophysiology and Natural History

Prostate cancer exhibits significant phenotypic heterogeneity, with a wide spectrum of latent to clinical disease.1 The effects and interaction of host and environmental risk factors (Table 1) with gonadal hormonal imbalances may determine the likelihood of development and progression of prostate cancer.

One hypothesis for development is that genetic factors and exposure to infectious agents result in injury of the prostate and lead to development of recurrent and chronic inflammation.1,2 These infectious agents include the sexually transmitted organisms Neisseria gonorrhoeae, Chlamydia trachomatis, Trichomonas vaginalis, and Treponema pallidum, and nonsexually transmitted bacteria that cause acute and chronic bacterial prostatitis, including Escherichia coli, papillomavirus, herpes simplex virus type 2, and cytomegalovirus.

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