7/27/2019 Mucinous Adenocarcinoma Prostate

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Mucinous adenocarcinoma ofthe prostate gland is one ofthe least common morphologic

variants ofprostatic carcinoma ( Epstein and Lieberman, 1985 ; Ro et al, 1990 ). It has an

aggressive biologic behavior and, like nonmucinousprostate carcinoma, has a propensity todevelop bone metastases and increased serum acid phosphatase and PSA levels with advanced

disease.

Even in ordinary adenocarcinomas oftheprostate without light microscopic evidence of

neuroendocrine differentiation, almost half show neuroendocrine differentiation on evaluation

with immunohistochemistry for multiple neuroendocrine markers ( di Sant'Agnese, 1992 ). Mostofthese neuroendocrine cells contain serotonin and, less frequently, calcitonin, somatostatin, or

human chorionic gonadotropin. Most ofthese cases have no evidence ofectopic hormonal

secretion clinically. Most studies do not demonstrate a convincing relation between the extent of

neuroendocrine differentiation in ordinaryprostate cancer and prognosis. Small cell carcinomasoftheprostate are identical to small cell carcinomas ofthe lung ( Tetu et al, 1987 ). In

approximately 50% ofthe cases, the tumors are mixed small cell carcinoma and adenocarcinoma

oftheprostate. Although most small cell tumors oftheprostate lack clinically evident hormone

production, they account for the majority ofprostatic tumors with clinically evidentadrenocorticotropic hormone or antidiuretic hormone production. The average survival ofpatients with small cell carcinoma ofthe prostate is less than a year. There is no difference inprognosis between patients with pure small cell carcinoma and those with mixed glandular andsmall cell carcinomas.

Between 0.4% and 0.8% ofprostatic adenocarcinomas arise from prostatic ducts ( Epstein andWoodruff, 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 symptomsor hematuria. Tumors arising in the more peripheral prostatic ducts may present like ordinary

(acinar) adenocarcinoma oftheprostate 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 andhave an aggressive course; they should be regarded as Gleason score 4+ 4 = 8 because oftheir shared cribriform morphologic features with acinar

adenocarcinoma Gleason score 8 and similar prognosis ( Brinker et al, 1999 ). Pure primary

squamous carcinoma ofthe 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 ofadenocarcinomas that

have been treated with estrogen therapy.