Literature DB >> 9008036

Two cases of small cell carcinoma of the prostate.

H Okada1, A Gotoh, T Ogawa, S Arakawa, C Ohbayashi, S Kamidono.   

Abstract

We describe the clinical and pathological findings in two Japanese men with small cell carcinoma of the prostate; case 1 was 58 years old and case 2 was 24 years old. Case 1 was initially diagnosed as a poorly differentiated adenocarcinoma of the prostate, stage D2, with marked elevation of serum neuron-specific enolase (NSE), carcinoembryonic antigen (CEA), and CA 19-9 levels. The patient had undergone castration and systemic chemotherapy. After three courses of chemotherapy, tumour markers were normalized. However, 6 months later serum levels of tumour markers again rose, and biopsy of the prostate revealed a small cell carcinoma component in the adenocarcinoma of the prostate and benign prostate hypertrophy. The patient was again treated with systemic chemotherapy but died within 1 year after relapse. In case 2, the patient presented with initial symptoms of lumbago and dysuria, and an enlarged prostate was radiologically diagnosed. Shortly after admission he developed ileus, and an exploratory laparotomy revealed a large tumour arising from the prostate and invading the peritoneal cavity. This tumour was pathologically diagnosed as a small cell carcinoma. The patient died shortly thereafter without responding to chemotherapy. Immunohistological evaluation was done using a panel of antibodies against NSE, chromogranin A, CEA, CA 19-9, prostatic acid phosphatase (PAP), prostate-specific antigen (PSA), leukocyte common antigen (LCA), epithelial membrane antigen (EMA), adrenocorticotropic hormone (ACTH), calcitonin, serotonin, gastrin, vasoactive intestinal peptide (VIP), and glucagon. CEA was intensely positive in the tumour lesions from case 1, and NSE and ACTH were focally positive, and calcitonin, serotonin, CA 19-9, and PSA were weakly positive only in several cells in the tumour lesions from case 1. In the tumour lesion from case 2, NSE was intensely positive, and chromogranin A was weakly positive. These findings support the neuroendocrine nature of this neoplasm.

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Year:  1996        PMID: 9008036     DOI: 10.3109/00365599609182334

Source DB:  PubMed          Journal:  Scand J Urol Nephrol        ISSN: 0036-5599


  2 in total

1.  Prostatic neuroendocrine tumor in multiple endocrine neoplasia Type 2B.

Authors:  B Goulet-Salmon; E Berthe; S Franc; S Chanel; F Galateau-Salle; M Kottler; J Mahoudeau; Y Reznik
Journal:  J Endocrinol Invest       Date:  2004-06       Impact factor: 4.256

Review 2.  Androgen-deprivation therapy-induced aggressive prostate cancer with neuroendocrine differentiation.

Authors:  Julia Lipianskaya; Alexa Cohen; Clark J Chen; Elaine Hsia; Jill Squires; Zhen Li; Yaqun Zhang; Wei Li; Xufeng Chen; Hua Xu; Jiaoti Huang
Journal:  Asian J Androl       Date:  2014 Jul-Aug       Impact factor: 3.285

  2 in total

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