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Prostate Cancer: Emerging Concepts: Part I

Marc B. Garnick, MD; and William R. Fair, MD
[+] Article and Author Information

From Beth Israel Hospital and Harvard Medical School, Boston, Massachusetts, and Memorial Sloan-Kettering Cancer Center, New York, New York. Requests for Reprints: Marc B. Garnick, MD, Beth Israel Hospital, Harvard Medical School, 330 Brookline Avenue, Boston, MA 02215. Current Author Addresses: Dr. Garnick: Beth Israel Hospital, 330 Brookline Avenue, Boston, MA 02215.


Copyright ©2004 by the American College of Physicians


Ann Intern Med. 1996;125(2):118-125. doi:10.7326/0003-4819-125-2-199607150-00008
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Objective: To review important topics related to prostate cancer that have arisen since this subject was last covered in Annals in 1993. The review consists of two parts. Part I describes advances in prostate-specific antigen (PSA) interpretation (including PSA density and velocity, age-specific reference ranges, “free” and “bound” PSA ratios, the utility of PSA in defining the pathologic extent of prostate cancer, and the use of these concepts in helping define appropriate treatment strategies), the management of patients with organ-confined prostate cancer, and pathologic interpretation of prostatectomy specimens.

Study Selection: Randomized studies identified through a MEDLINE search (1992 to 1996); large, single-institution conferences and consortiums; and studies presented at regional, national, and international symposia.

Data Synthesis: Both qualitative and quantitative data are reported. Most of the data presented in part I concern advances in the interpretation of PSA results and characterization of the pathologic findings of prostatectomy specimens. Studies show that almost 50% of patients with clinically organ-confined prostate cancer have disease that is beyond the confines of the prostatic capsule. The chances of developing clinical (radiographic) and biochemical failure (that is, elevation of PSA levels) are 3% and 6%, respectively, for pathologically organ-confined cancer and 10% and 26%, respectively, for non-specimen-confined prostate cancer. Actual progression-free survival rates 10 years after radical prostatectomy are 70% for patients with organ-confined cancer and 39% for patients with cancer that has spread through the capsule.

Conclusions: Prostate cancer is being detected with increasing frequency, and many patients with this condition are receiving such treatments as radical prostatectomy and radiation therapy. Although refinements in PSA-based testing have contributed substantially to the increased detection rate of prostate cancer, the incidence of disease was increasing dramatically even before the detection of PSA was possible. Yet, despite earlier detection, the optimal therapy for the early form of the disease remains enigmatic. Further studies and longer follow-up of patients who participated in completed studies are needed to better define the outcomes of prostate cancer therapies and to help determine the importance of the therapies. Increased research efforts are necessary to help elucidate the reasons for the great increase in the incidence of the disease; such efforts should help define strategies to ultimately prevent prostate cancer.

Figures

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Figure 1. Incidental cancers include stage A and T1 cancers, indicating that the cancer was not palpable on physical examination before prostate biopsy. Stage T1c indicates that no palpable abnormality was seen on digital rectal examination. Organ-confined cancers include stage B and T2 lesions and are generally thought to be confined to the prostate gland. Locally invasive cancers or regional cancers include stage C and T3 and T4 lesion. Before radical prostatectomy, patients are assigned a clinical stage of cancer in the TNM system; this classification is generally signified by a “c” that precedes the T stage. Thus, a cT2b cancer is thought to be confined to one lobe of the prostate gland. After radical prostatectomy, a pathologic stage (as determined by the pathologic findings) is assigned to the cancer; this classification is generally indicated by a “p” that precedes the T stage. Thus, a patient who has cT2b cancer could have pT3c cancer if more extensive disease is detected in the final prostatectomy specimen than was appreciated on clinical evaluation. If nodal tissue is removed and examined after prostatectomy, a description of nodal status (positive or negative) will also be assigned to the cancer. Disseminated disease includes stage D and N+ or M+ cancers, indicating that the cancer has spread to the lymph nodes or other visceral sites.
Comparison of the older Whitmore-Jewett classification system for prostate cancer with the tumor, node, metastases (TNM) system.
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