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Risk Factors for Prostate Cancer

Kenneth J. Pienta, MD; and Peggy S. Esper, MSN
[+] Article and Author Information

From the Meyer L. Prentis Comprehensive Cancer Center of Metropolitan Detroit, The Wayne State University School of Medicine, Detroit, Michigan. Requests for Reprints: Kenneth J. Pienta: Room 213, Michigan Cancer Foundation, 110 E. Warren, Detroit, MI 48201. Acknowledgments: The authors thank Drs. Ray Demers, Linda Smith, and Judy Karp for their critical review and R. Demers, L. Smith, and T.Y. Kao for contribution of the metropolitan Detroit 1991 SEER data. Grant Support: In part by the Wayne State University Fund for Medical Research and Education and through National Cancer Institute SEER contract NO1-CN-05225. Dr. Pienta is supported by Physician Scientist Award CA 60156.


Copyright 2004 by the American College of Physicians


Ann Intern Med. 1993;118(10):793-803. doi:10.7326/0003-4819-118-10-199305150-00007
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Purpose: To review the current state of knowledge regarding risk factors for prostate cancer.

Data Sources: Analysis of the literature through the use of MEDLINE as well as identification of papers through review of article bibliographies and the authors' personal files. Current data were also extracted from the Surveillance, Epidemiology, and End Results Program (SEER) database.

Data Selection: A review of risk factors for the development of prostate cancer. Emphasis was placed on identifying larger, controlled studies.

Data Synthesis: The clinical incidence of prostate cancer is increasing. Risk factors for prostate cancer appear to include age, race, positive family history, vasectomy, and dietary fat intake.

Conclusions: It appears that prostate cancer results from an interplay between endogenous hormones and environmental influences that include, most prominently, dietary fat.

Figures

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Figure 1.
Age-adjusted death rates due to prostate cancer per 100 000 population.[7]

(From Boring and colleagues .).

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Figure 2.
Comparison of the age-specific prevalence of prostate cancer in the United States and Japan.Top panel.Bottom panel.[1]

Histologic prostate cancer. Clinical prostate cancer. (From Carter and colleagues .).

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Figure 3.
Prostate cancer incidence rates for the years 1973 to 1990.

Rates are shown for the tricounty metropolitan Detroit area as measured by the Surveillance, Epidemiology, and End Results (SEER) program. Rates are per 100000, are age-adjusted to the 1970 U.S. standard population, and are representative of new cancer cases diagnosed in a given year.

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Figure 4.
Incidence rates by age and race for invasive prostate cancer.

Rates are shown for metropolitan Detroit tricounty residents in 1989 as reported by the SEER data base. Rates are per 100000 and are age adjusted to the 1970 U.S. standard population.

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Figure 5.
The positive correlation between breast and prostate cancer by country.[131]

The incidence of both breast and prostate cancer is higher in more developed countries. These data suggest that environmental influences may be important in the promotion of these diseases (see text). (From Rose and colleagues .).

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Figure 6.
The positive correlation between the mortality rate for prostate cancer and animal fat consumption by country.[131]

These data suggest that high fat intake may be related to the risk for developing prostate cancer (see text). (From Rose and colleagues .).

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Figure 7.
Potential sites of intervention for prostate cancer treatment and prevention.[13]

A better understanding of the interplay of multiple hormones as well as other factors with the prostate will allow the potential design of new therapeutic strategies to intervene in the process of prostate carcinogenesis. Epidemiologic studies provide important clues in understanding the factors important in the development of prostate cancer. (Adapted from Coffey and Pienta ). ACTH = adrenocorticotropin releasing hormone; CNS = central nervous system; CRH= corticotropin releasing hormone; DHT = dihydrotestosterone; FSH = follicle stimulating hormone; FSH-RH = follicle stimulating hormone releasing hormone; LH = luteinizing hormone; LH-RH = luteinizing hormone releasing hormone; S = seminiferous; T = testosterone.

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