Final Diagnosis -- Prostatic Adenocarcinoma





Carcinoma of the prostate is the most common form of cancer in men and the second leading cause of cancer death in the United States. It is a disease of elderly men. Only 1% of prostate cancers is diagnosed before 50 years of age. The age-adjusted incidence in the United States is 69 per 100,000. The disease is even more prevalent among African Americans. However, prostate cancer is extremely rare in Asian. Little is know about the causes of prostatic cancer. Multiple factors have been speculated such as age, race, family history, hormone levels, and environmental influences (4). In approximately 10% of white American men, the development of prostate cancer has been linked to prostate cancer susceptibility genes. In one third of these familiar cases, a gene has been mapped to chromosome 1q24-25 (16).

Conventional (acinar) adenocarcinoma represents the large majority (as much as 95%) of the prostatic cancers (10). Uncommon carcinomas of prostate include squamous cell carcinoma, adenosquamous carcinoma, transitional cell carcinoma, and rare variants of adenocarcinoma including mucinous (colloid) carcinoma, cribriform carcinoma, adenocarcinoma with signet ring differentiation, adenoid cystic-like carcinoma, small cell carcinoma, sarcomatoid carcinoma, carcinosarcoma, and prostate duct adenocarcinoma (PDA).

Melicow and Pachter (8) first described a case of PDA (also known as large duct adenocarcinoma or endometrioid adenocarcinoma of the prostate) in 1967. The incidence of PDA has been reported to vary from 0.2 % (12) to 1.3 % (3) among all prostatic carcinoma. It occurs in the patients of age (mean age 65 years, 10) similar as for conventional acinar adenocarcinoma.

PDA has been a source of conflict and debate over the years regarding its origin. Despite earlier arguments that the so-called "endometrioid carcinoma of prostate" is of Mullerian remnant origin (8), many studies (11) indicate that PDA is actually an adenocarcinoma of primary prostatic duct origin (5, 9, 10). Ultrastructural studies (2, 14) also support a prostatic origin.

The periurethral PDA lesions may present with urinary obstruction and hematuria. Peripheral lesions present symptoms same as conventional acinar adenocarcinoma, for example, prostatism, urgency, and frequency. The periurethral lesions may be visible at cystoscopy as a villous or papillary lesion around the verumontanum. Serum PSA and PAP values may be normal or raised (9).

The gross appearance of PDA is usually friable exophytic urethral lesions with polypoid or papillary configuration (15). It may also arise in peripheral prostate with prostatic enlargement. The typical microscopic appearance of PDA shows tall pseudostratified or stratified columnar epithelial cells, usually with amphophilic cytoplasm, either lining papillary fronds, or forming cribriform glands with slit-like lumina, or individual glands. There is also possibly extensive comedonecrosis and striking nuclear pleomorphism. Variants can have solid areas or clear cytoplasm. Approximately 50% of PDA also contain foci of acinar differentiation (9). The associated micro-acinar carcinoma tends to be poorly differentiated carcinoma of high Gleason score. Sometimes, PDA may be difficult to distinguish from high grade PIN or transitional cell carcinoma. It has two histologic growth patterns; type A, an exuberant papillary endometrioid pattern with a focal intraductal component, and type B, less papillary-endometrioid growth and more intraductal components.

Cytology sample of PDA shows clusters of malignant cells with crowding and overlapping of hyperchromatic nuclei containing prominent nucleoli; and with loss of polarity and cohesion. Tumor cells typically has a pseudopapillary pattern but occasionally may be mixed with flat sheets of tumor cells. In 10 % of cases, grooved nuclei in tumor cells similar to those observed in papillary carcinoma of the thyroid are noted (7).

Immunohistochemical staining of this tumor for PSA and PAP is usually strongly positive (6). Ultrastructural study will identify prostatic epithelial cells rather than ciliated endometrial features. PDA may also show positivity for high-molecular weight cytokeratin as it grows into ducts.

Treatment of PDA involves a variety of courses and has tended to be similar to that used for conventional prostatic acinar carcinoma (9). The clinical behavior and prognosis of PDA are still unknown. Some studies demonstrated the prognosis of PDA to be worse than conventional adenocarcinoma (5, 13, 2, 11, and 12), and it does not respond as well to hormonal therapy. However, in recent follow-up studies (1, 9), the PDA of pure ductal carcinoma (without mixture of high grade micro-acinar carcinoma) responds well to orthodox micro-acinar carcinoma therapy including TURP and orchiectomy. It also appears sensitive to hormonal manipulation. Therefore, the pure form of PDA of prostate may have a good prognosis.


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  15. . Zarifis I. et al. (1993) Re: Endometrioid carcinoma of the prostate. The diagnostic value of Leu7 and prostatic specific antigen. N. E. Stavropoulos et al. Br. J. Urol., 71, 309-312, 1993 [letter]. British Journal of Urology 72(5 Pt 1):673.
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Contributed by Wen-Wei Chung, MD, PhD and Rajiv Dhir, MD


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