Significance
Incidence and Mortality
Risk Factors
Incidence and Mortality
Prostate cancer is the most common cancer diagnosed in North American men, excluding skin cancers. It is estimated that in 2008, approximately 186,320
new cases and 28,660 prostate cancer-related deaths will occur in the United
States.[1]. Prostate cancer is now the second leading cause of cancer death in
men, exceeded only by lung cancer. It accounts for 25% of all male cancers and
10% of male cancer-related deaths.[1] Age-adjusted incidence rates increased
steadily over the past several decades, with particularly dramatic increases associated with
the inception of widespread use of prostate-specific antigen (PSA) screening in the late
1980s and early 1990s, followed by a more recent fall in incidence.
Age-adjusted mortality rates have recently paralleled incidence rates, with an
increase followed by a decrease in the early 1990s.[2] It has been suggested
that declines in mortality rates in certain jurisdictions reflect the
benefit of PSA screening,[3] but others have noted that these
observations may be explained by independent phenomena such as improved
treatment effects.
Regional differences have been observed in prostate cancer incidence and mortality rates and in rates of radical prostatectomy. The increased
incidence until 1989 was most likely the result of increased tumor detection due to increasing rates of transurethral prostatectomy.[4,5] Subsequent
increases were most likely the result of widespread use of PSA testing for early detection and
screening.[6,7] Variable incidence rates may reflect variability in the
intensity of early detection practices across the United States and other
jurisdictions. While differences in aggregate mortality by regions of the
United States have not been observed, considerable variation in mortality rates
between African American and white men are seen.[8,9] (Refer to the Population Observations on Early Detection, Incidence, and Prostate Cancer Mortality section of this summary for more information.)
Risk Factors
Prostate cancer is uncommonly seen in men younger than 50 years; the
incidence rises rapidly with each decade thereafter. The age-adjusted
incidence is higher in African American males (258.3 per 100,000) than in
white males (163.4 per 100,000).[10] African American males have a higher
mortality from prostate cancer, even after attempts to adjust for
access-to-care factors.[11] Men with a family history of prostate cancer are
at an increased risk of the disease compared with men without this history.[12,13]
Other potential risk factors besides age, race, and family history of prostate
cancer include alcohol consumption, vitamin or mineral interactions, and other
dietary habits.[14-18] A significant body of evidence suggests that a diet high in fat, especially saturated fats and fats of animal origin, is associated with a higher risk of prostate cancer.[19,20] Other possible dietary influences include selenium, vitamin E, vitamin D, lycopene, and isoflavones. (Refer to the PDQ summary on Prostate
Cancer Prevention for more information.) Evidence from a nested case-control study within the
Physicians’ Health Study,[21] in addition to a case-control study [22] and a retrospective review of screened prostate cancer patients,[23] suggests that higher plasma insulin-like growth
factor-I levels may be associated with a higher prostate cancer risk.[24] Not all studies, however, have confirmed this association.[25]
The estimated lifetime risk of diagnosis of prostate cancer is about 17.1%, and the lifetime risk of dying from this disease is 2.9%.[10]
The biology and natural history of prostate cancer is not completely understood. Rigorous evaluation of any prostate cancer screening modality is desirable because the natural history of the disease is variable, and appropriate treatment is not clearly defined. Although the prevalence of prostate cancer and preneoplastic lesions found at
autopsy steadily increases for each decade of age, most of these lesions remain
clinically undetected.[26]
There is an association between primary tumor volume and
local extent of disease, progression, and survival.[27] A review of a large
number of prostate cancers in radical prostatectomy, cystectomy, and autopsy
specimens showed that capsular penetration, seminal vesicle invasion, and lymph
node metastases were usually found only with tumors larger than 1.4 cc.[28]
Furthermore, the semiquantitative histopathologic grading scheme proposed by
Gleason is reasonably reproducible among pathologists and correlates with the
incidence of nodal metastases and with patient survival in a number of reported
studies.[29]
Cancer statistics from the American Cancer Society and the National Cancer
Institute indicated in 2004 that the proportion of disease diagnosed at a
locoregional stage and at a distant stage is 91% and 5% for whites, compared with 89%
and 7% for African Americans, respectively.[30] Stage distribution of prostate cancer is affected
substantially by the intensity of early detection efforts.
Pathologic stage does not always reflect clinical stage and upstaging (owing
either to extracapsular extension, positive margins, seminal vesicle invasion, or
lymph node involvement) occurs frequently. Of the prostate cancers detected by
digital rectal exam (DRE) in the pre-PSA era, 67% to 88% were at a
clinically localized stage (T1–2 Nx M0 [T = tumor size, N = lymph node involvement, and M = metastasis]).[31,32] However, in one of those series
of 2,002 patients undergoing annual screening DRE, only
one-third of men proved to have pathologically organ-confined disease.[32]
With the proliferation of PSA for early detection, reviews of large numbers of
asymptomatic men with prostate cancer found that most have organ-confined disease. One study found
that 63% of cancers detected in men undergoing their first screening PSA were
pathologically organ-confined cancers; the percentage increased to 71% if
cancer was detected on a subsequent examination.[33] In a series of 2,999 men
undergoing screening with PSA, DRE, and transrectal ultrasound, 62% of the
tumors detected were reported to be pathologically organ-confined.[34] While
the proportion of node-positive cancers in the pre-PSA era were in the range of
25% for patients with ostensibly localized disease, current series report
proportions as low as 3%.[35] Stage T1c tumors detected by serial PSA and
removed by radical prostatectomy are organ-confined in 79% of cases.[36]
Survival rates for prostate cancer have improved from 1974 to the present.
Lead-time and length-bias effects of early detection and the possible influence
of stage migration must also be considered when trends in survival
data are interpreted.[37] Reported survival rates may also vary, depending on whether the analytical methods reflect crude disease-specific rates (absolute
disease-specific survival) or take into account competing risks for the given
age group (relative disease-specific survival).
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