We previously reported a substantial decline in early-stage prostate cancer incidence rates from 2011 to 2012 in men 50 years or older residing in areas covered by the population-based Surveillance, Epidemiology, and End Results (SEER) program.1 This pattern coincided with the decline in prostate-specific antigen (PSA) testing in this age group between 2010 and 2013 following the US Preventive Services Task Force recommendation against routine PSA testing in all men in October 2011 in draft form and in May 2012 in final form, which was preceded by a 2008 recommendation against PSA testing in men 75 years or older.2 Whether the decrease in incidence rates persisted through 2013 is unknown.
The study was based on a deidentified publicly available database and did not require institutional review board review. We obtained incidence data for invasive prostate cancer diagnosed from 2005 through 2013 in men 50 years and older in 18 SEER registries, covering approximately 28% of the US population.3 Cases were categorized as local/regional or distant stage according to SEER summary stage.4(p226) We calculated delay-adjusted incidence rates by age (≥50 years, 50-74, ≥75 years), stage (all stages, local/regional, distant), and race/ethnicity (all races, non-Hispanic whites, non-Hispanic blacks) using SEER*Stat software.3 Rates were age standardized to the 2000 US population and expressed per 100 000 men. Incidence ratios (IRs) and their 99% confidence intervals measuring the relative change in incidence rates between consecutive years (eg, 2005 vs 2006) were calculated using the method of Tiwari et al.5
From 2012 to 2013, localized/regional-stage prostate cancer incidence rates per 100 000 men significantly decreased from 356.5 to 335.4 (IR, 0.94; 99% CI, 0.92-0.96) in men aged 50 to 74 years and from 379.2 to 353.6 (IR, 0.93; 99% CI, 0.89-0.97) in men aged 75 years and older (Figure 1). In contrast, incidence rates for distant-stage disease during the corresponding period remained unchanged in both men aged 50 to 74 years (from 15.7 to 16.5; IR, 1.05; 99% CI, 0.96-1.15) and 75 years and older (from 65.8 to 66.4; IR, 1.01; 99% CI, 0.91-1.12) (Figure 2). We found similar results in non-Hispanic whites and non-Hispanic blacks, although the decrease for early-stage disease in blacks was not statically significant, possibly due to lack of statistical power (data not shown).
Incidence rates for early-stage prostate cancer continued to decline in men 50 years and older in the 18 SEER areas following the US Preventive Services Task Force recommendations against routine PSA testing to all men in 2012, although the decrease from 2012 to 2013 was smaller than that from 2011 to 2012 (6% vs 19%). Simultaneously, as reported before, PSA testing rates between 2010 and 2013 in the United States significantly decreased from 36.8% (99% CI, 34.3%-39.4%) to 29.9% (99% CI, 28.0%-32.0%) in men 50 to 74 years old and from 43.1% (99% CI, 37.1%-49.2%) to 36.3% (99% CI, 31.1%-41.9%) in men 75 years and older.1
Other factors that may have contributed to the decrease in incidence rates for early-stage prostate cancer include changes in the prevalence of risk factors and/or preventive measures. However, as noted in our previous article,1 temporal changes in established risk factors (age, race/ethnicity, and family history) are unlikely to have caused the continued decrease in the incidence rates. Although 5α-reductase inhibitor treatment has been shown to reduce the risk of prostate cancer,6 their use is not recommended for prevention in the general population.
In conclusion, the decrease in early-stage prostate cancer incidence rates from 2011 to 2012 in men 50 years and older persisted through 2013 in SEER registries, albeit at a slower pace. Whether this pattern will lead to a future increase in the diagnosis of distant-stage disease and prostate cancer mortality requires long-term monitoring because of the slow-growing nature of this malignant neoplasm.
Corresponding Author: Ahmedin Jemal, DVM, PhD, Surveillance and Health Services Research, American Cancer Society, 250 Williams St NW, Atlanta, GA 30345 (ajemal@cancer.org).
Published Online: August 18, 2016. doi:10.1001/jamaoncol.2016.2667
Author Contributions: Dr Ma had full access to all of the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis.
Study concept and design: Jemal, Brawley, Ward.
Acquisition, analysis, or interpretation of data: Jemal, Ma, Siegel, Fedewa.
Drafting of the manuscript: Jemal.
Critical revision of the manuscript for important intellectual content: All authors.
Statistical analysis: Ma.
Administrative, technical, or material support: Jemal, Fedewa, Brawley.
Study supervision: Jemal, Brawley, Ward.
Conflict of Interest Disclosures: None reported.
Funding/Support: This project was supported by the Intramural Research Department of the American Cancer Society.
Role of the Funder/Sponsor: The American Cancer Society had no role in the design and conduct of the study; collection, management, analysis, and interpretation of the data; preparation, review, or approval of the manuscript; and decision to submit the manuscript for publication.
Disclaimer: The opinions expressed are solely the responsibility of the authors and do not necessarily reflect the official views of the American Cancer Society.
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