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  • Prostate cancer is a malignant neoplasm that arises from the prostate gland. Prostate cancer has an indolent course; localized prostate cancer is curable by surgery or radiation therapy, but advanced prostate cancer is not yet curable.


  • The normal prostate is composed of acinar secretory cells that are altered when invaded by cancer. The major pathologic cell type is adenocarcinoma (>95% of cases).

  • Prostate cancer can be graded. Well-differentiated tumors grow slowly, whereas poorly differentiated tumors grow rapidly and have a poor prognosis.

  • Metastatic spread can occur by local extension, lymphatic drainage, or hematogenous dissemination. Skeletal metastases from hematogenous spread are the most common sites of distant spread. The lung, liver, brain, and adrenal glands are the most common sites of visceral involvement, but these organs are not usually involved initially.

  • The rationale for hormone therapy is based on the effect of androgens on the growth and differentiation of the normal prostate (Fig. 64–1).

  • The testes and the adrenal glands are the major sources of androgens, specifically dihydrotestosterone (DHT).

  • Luteinizing hormone–releasing hormone (LHRH) from the hypothalamus stimulates the release of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) from the anterior pituitary gland.

  • LH complexes with receptors on the Leydig cell testicular membrane, stimulating the production of testosterone and small amounts of estrogen.

  • FSH acts on testicular Sertoli cells to promote maturation of LH receptors and produce an androgen-binding protein.

  • Circulating testosterone and estradiol influence the synthesis of LHRH, LH, and FSH by a negative-feedback loop at the hypothalamic and pituitary level.

FIGURE 64–1.

Hormonal regulation of the prostate gland.

(ACTH, adrenocorticotropic hormone; DHT, dihydrotestosterone; FSH, follicle-stimulating hormone; GH, growth hormone; LH, luteinizing hormone; LHRH, luteinizing hormone–releasing hormone; mRNA, messenger RNA; PROL, prolactin; R, receptor.)


  • The risk of prostate cancer was reduced approximately 25% in patients taking finasteride for treatment of benign prostatic hypertrophy (BPH), but prostate cancer diagnosed in patients on finasteride is more aggressive.

  • Current guidelines do not recommend the use of finasteride or dutasteride for prostate cancer chemoprevention. Although finasteride reduces the prevalence of prostate cancer, the impact on prostate cancer morbidity or mortality has not been demonstrated.


  • Screening for prostate cancer is controversial. The American Urologic Association does not recommend routine screening in men between the ages of 40 and 54 years of average risk. They recommend that men aged 55 to 69 years discuss the risks and benefits of prostate cancer screening. Men who elect screening should do so no more than every 2 years; a recent study suggests that screening every 5 years may be adequate.

  • PSA is a glycoprotein produced and secreted by prostate epithelial cells. Acute urinary retention, acute prostatitis, and BPH influence PSA, thereby limiting the usefulness of PSA alone for early ...

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