Mucinous adenocarcinoma of the prostate gland is one of the least common morphologic variants of prostatic carcinoma ( Epstein and

Lieberman, 1985 ; Ro et al, 1990 ). It has an aggressive biologic behavior and, like nonmucinous prostate carcinoma, has a propensity to develop bone metastases and increased serum acid phosphatase and PSA levels with advanced disease. Even in ordinary adenocarcinomas of the prostate without light microscopic evidence of neuroendocrine differentiation, almost half show neuroendocrine differentiation on evaluation with immunohistochemistry for multiple neuroendocrine markers ( di Sant'Agnese, 1992 ). Most of these neuroendocrine cells contain serotonin and, less frequently, calcitonin, somatostatin, or human chorionic gonadotropin. Most of these cases have no evidence of ectopic hormonal secretion clinically. Most studies do not demonstrate a convincing relation between the extent of neuroendocrine differentiation in ordinary prostate cancer and prognosis. Small cell carcinomas of the prostate are identical to small cell carcinomas of the lung ( Tetu et al, 1987 ). In approximately 50% of the cases, the tumors are mixed small cell carcinoma and adenocarcinoma of the prostate. Although most small cell tumors of the prostate lack clinically evident hormone production, they account for the majority of prostatic tumors with clinically evident adrenocorticotropic hormone or antidiuretic hormone production. The average survival of patients with small cell carcinoma of the prostate is less than a year. There is no difference in prognosis between patients with pure small cell carcinoma and those with mixed glandular and small cell carcinomas. Between 0.4% and 0.8% of prostatic adenocarcinomas arise from prostatic ducts ( Epstein and Woodruff, 1986 ; Christensen et al, 1991 ). When prostatic duct adenocarcinomas arise in the large primary periurethral prostatic ducts, they may grow as an exophytic lesion into the urethra, most commonly in and around the verumontanum, and give rise to either obstructive symptoms or hematuria. Tumors arising in the more peripheral prostatic ducts may present like ordinary (acinar) adenocarcinoma of the prostate and may be diagnosed on needle biopsy ( Brinker et al, 1999 ). Tumors are often underestimated clinically because rectal examination findings and serum PSA levels may be normal. Most prostatic duct adenocarcinomas are advanced stage at presentation and have an aggressive course; they should be regarded as Gleason score 4 + 4 = 8 because of their shared cribriform morphologic features with acinar adenocarcinoma Gleason score 8 and similar prognosis ( Brinker et al, 1999 ). Pure primary squamous carcinoma of the prostate is rare and is associated with poor survival ( Parwani et al, 2004 ). These tumors develop osteolytic metastases, do not respond to estrogen therapy, and do not develop elevated serum acid phosphatase levels with metastatic disease. More commonly, squamous differentiation occurs in the primary and metastatic deposits of adenocarcinomas that have been treated with estrogen therapy.