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Query: UMLS:C0007112 (prostatic adenocarcinoma)
 2,574 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Because small cell anaplastic carcinoma of the prostate is an uncommon tumor, it has remained a poorly defined entity. To elucidate further the clinical, pathological and immunohistochemical characteristics of this cancer the 27 patients who presented to the Mayo Clinic from 1960 to 1990 were reviewed. Of these patients 18 (67%) presented with pure small cell anaplastic carcinoma, and 9 (33%) were diagnosed with small cell anaplastic carcinoma and adenocarcinoma of the prostate. Twenty-six patients (96%) had either stage C or D disease at the time of diagnosis. Two patients presented with a paraneoplastic syndrome, including 1 man with inappropriate antidiuretic hormone secretion and 1 who suffered from thyroxine intoxication. Of 24 men with long-term followup 22 (92%) died of small cell anaplastic carcinoma of the prostate despite antiandrogen therapy and the remaining 2 are alive with active, progressive disease. The median survival time following diagnosis was 17.1 months (range 2 to 90 months). All tumors with tissue available for immunohistochemical staining reacted positive for neuron-specific enolase, indicating that small cell anaplastic carcinoma of the prostate is most likely a neuroendocrine neoplasm. No tumor stained positive for either prostatic acid phosphatase or prostate specific antigen. Pathologically, small cell anaplastic carcinoma of the prostate appears to be similar to oat cell carcinoma of the lung. This series of 27 patients emphasizes that small cell anaplastic carcinoma of the prostate is highly malignant, is frequently of advanced stage at presentation, responds poorly to antiandrogen therapy and has a poor prognosis.
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PMID:Small cell anaplastic carcinoma of the prostate: a clinical, pathological and immunohistological study of 27 patients. 131 95

Endocrine-paracrine cells of the prostate (also known as APUD or neuroendocrine cells) constitute, in addition to the basal and exocrine secretory cells, a third population of highly specialized epithelial cells in the prostate gland. These endocrine-paracrine cells contain, and most likely secrete, serotonin and calcitonin, as well as variety of other peptides. Little is known of the functional role of these cells, but they probably subserve a paracrine or local regulatory role. They may also regulate via endocrine, lumencrine, or neurocrine mechanisms. These endocrine-paracrine cells probably play a significant role during prostatic growth and differentiation as well as regulating the secretory process of the mature gland. Neuroendocrine differentiation in prostatic carcinoma occurs in the form of the relatively rare small cell carcinoma and carcinoid or carcinoid-like tumor, but most commonly as focal neuroendocrine differentiation in a conventional prostatic adenocarcinoma that is a very frequent, if not ubiquitous phenomenon, and reflects tumor cell heterogeneity mimicking the normal differentiation process. The world's literature on neuroendocrine differentiation in prostatic carcinoma is reviewed. Neuroendocrine differentiation in all types of prostatic carcinoma appears to correlate with a poor prognosis. This correlation is probably multifactorial and may relate to a positive correlation with grade, a direct resistance to hormonal manipulation, and/or autocrine/paracrine growth factor activity due to the secretion of neuroendocrine products. Neuron-specific enolase and chromogranin, as well as other neuroendocrine products, may be useful as serum markers in patients with prostatic carcinoma with neuroendocrine differentiation. New therapeutic strategies need to be developed to treat these tumors. This includes the use of specialized protocols that have been effective against neuroendocrine carcinomas arising in other organ systems.
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PMID:Neuroendocrine differentiation in carcinoma of the prostate. Diagnostic, prognostic, and therapeutic implications. 135 Sep 41

Paneth cell-like change (PCLC) of the prostatic glandular epithelium was focally observed in one case of normal glandular epithelium, two cases of glandular and stromal hyperplasia, one case of prostatic intraepithelial neoplasia, and four cases of prostatic adenocarcinoma. The distinctive cells were characterized by bright, eosinophilic cytoplasmic granules on routine hematoxylin and eosin-stained material. The cytoplasmic granules in the benign prostatic epithelium were periodate-Schiff's procedure (PAS)-positive and diastase resistant and immunohistochemically negative for lysozyme, neuron-specific enolase, chromogranin, and serotonin. The eosinophilic granules in the prostatic intraepithelial neoplasia and adenocarcinoma cases were immunohistochemically positive for chromogranin, serotonin, and neuron-specific enolase, and negative for lysozyme. By electron microscopy the eosinophilic granules represented exocrine-like or lysosomal-like vesicles in the benign epithelium and neuro-endocrine granules in the malignant epithelium. The lesion represents a prostatic epithelial PCLC rather than a Paneth cell metaplasia. PCLC is the common histological manifestation of two different phenomena: (a) a PAS-positive and diastase-resistant eosinophilic cytoplasmic granular change in benign prostatic epithelium, and (b) endocrine differentiation with neuroendocrine granules in dysplastic and malignant prostatic epithelia. The importance of recognizing PCLC lies in its differentiation from other possible prostatic cytoplasmic inclusions.
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PMID:Paneth cell-like change of the prostate gland. A histological, immunohistochemical, and electron microscopic study. 137 Jan 93

A case of mucinous adenocarcinoma of the prostate that was diagnosed with the aid of prostate-specific antigen immunoperoxidase staining is reported. Focal areas of the tumor, which were morphologically similar to the remainder of the tumor, stained with neuron-specific enolase by an immunoperoxidase technique and with the Grimelius stain. This tumor is best thought of as a variant of the classic acinotubular adenocarcinoma of the prostate with well-differentiated cells that secrete mucin, rather than as a completely different type of cancer, as proposed previously.
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PMID:Mucinous adenocarcinoma of the prostate. 242 79

A fifty-eight-year-old white man was diagnosed as having an adenocarcinoma of the prostate (grade III by the U.T.M.D. Anderson Hospital grading system). Five years after the initial diagnosis and three months after signs and symptoms of the myasthenic syndrome of Eaton-Lambert (MSEL), he was found to have a small cell carcinoma of the prostate. Histologic examination showed adenocarcinoma merging into a small cell carcinoma component of intermediate cell type. Immunostaining was positive for neuroendocrine markers--namely, neuron-specific enolase and serotonin--and was limited to the small cell carcinoma component. This is the first report of a patient with small cell carcinoma of the prostate presenting with MSEL. Our findings support prior observations of a strong propensity for small cell carcinoma to be associated with paraneoplastic syndromes, regardless of the initial location of the tumor.
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PMID:Small cell carcinoma of prostate associated with myasthenic (Eaton-Lambert) syndrome. 253 72

In recent years many new and improved cancer markers have become available. From a clinical point of view, the most useful of the new markers include CA 19-9 for pancreatic adenocarcinoma, CA 125 for epithelial ovarian cancer, CA 15-3 for breast cancer, prostate specific antigen for prostatic adenocarcinoma, placental alkaline phosphatase for testicular seminomas and neuron-specific enolase for small cell carcinoma of lung. None of these new markers are specific for cancer. Furthermore, none are organ specific, except prostate specific antigen for prostatic tissue. The main application of these markers is in monitoring patients with the specific malignancies indicated. Whether routine use of any of these new markers leads to higher quality of life or enhanced survival remains to be determined.
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PMID:New cancer markers. 268 69

Specimens from 53 cases of prostatic carcinoma obtained during total prostatectomy or transurethral resection of prostate were analyzed for neuroendocrine differentiation with immunocytochemical tests for serotonin, neuron-specific enolase, and chromogranin as well as with the Churukian-Schenk argyrophil reaction. Forty-seven per cent (25 of 53) of the prostatic carcinomas were positive for neuroendocrine differentiation, usually with an overlapping combination of these techniques. Nine per cent (five cases) contained areas with numerous neuroendocrine cells, 11 per cent (six cases) had focal scattered neuroendocrine cells, and 26 per cent (14 cases) had rare neuroendocrine cells. The positive cases spanned the histologic spectrum of prostatic adenocarcinoma; histologically none resembled a carcinoid tumor or a small cell carcinoma. Positive cases were further studied with a battery of antisera to 12 polypeptide hormones. Immunoreactivity to only bombesin (one case) and calcitonin (two cases) was detected. In five cases, neuroendocrine differentiation was studied by electron microscopy and verified at the ultrastructural level.
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PMID:Neuroendocrine differentiation in prostatic carcinoma. 361 Jan 35

Paneth cell-like change (PCLC) of the prostatic epithelium is considered to be a distinct form of neuroendocrine differentiation characterized by isolated cells or small groups of cells with prominent eosinophilic cytoplasmic granules. We evaluated 300 serially sectioned radical prostatectomy specimens from patients with prostatic adenocarcinoma who had not received prior adjuvant therapy (pathologic stages T2NOMO [177 patients], T3NOMO [100 patients], and TxN1MO [23 patients]). Paneth cell-like change was identified in 30 cases (10%), ranging from 1 to 20 high-power fields/positive case (mean, 4.1 high-power fields/case). There was no correlation of PCLC with prostate volume, prostate weight, Gleason grade, nuclear grade, lymph node metastases, serum prostate-specific antigen levels, cancer volume, area or presence of capsular perforation, seminal vesicle invasion, or glandular mucin (all P > .05), although a positive correlation was seen with cribriform pattern (r = 0.50, P = .0015). Immunohistochemistry revealed cytoplasmic immunoreactivity within cells of PCLC for chromogranin (seven of seven cases), neuron-specific enolase (seven of seven cases), serotonin (six of seven cases), prostate-specific antigen (five of seven cases), and prostatic acid phosphatase (four of seven cases); lysozyme was negative (seven cases). Our findings indicate that PCLC is more common than previously reported, but that it is not associated with tumor grade, serum PSA levels, or pathologic stage. This study also shows that PCLC represents neuroendocrine differentiation, suggesting that the term "Paneth cell-like change" be deleted from the pathologist's lexicon in relation to prostatic adenocarcinoma; a more appropriate term might be "neuroendocrine cells with large eosinophilic granules."
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PMID:Paneth cell-like change in prostatic adenocarcinoma represents neuroendocrine differentiation: report of 30 cases. 811 11

Neuroendocrine cells are thought to have a regulatory role in prostatic epithelial growth and may be prognostically useful in prostatic adenocarcinoma. To determine the extent of neuroendocrine differentiation in high-grade prostatic intraepithelial neoplasia (PIN), a putative precursor of cancer, we studied the immunohistochemical expression of 10 markers in 26 radical prostatectomy specimens with PIN and adenocarcinoma. Expression was measured as mean percent of positive cases and positive high-power (x40) fields. The highest percentage of cases showed immunoreactivity for serotonin (73%, PIN; 54%, carcinoma), neuron-specific enolase (NSE) (67%, PIN; 46%, carcinoma), chromogranin (62%, PIN; 65%, carcinoma), and human chorionic gonadotropin (hCG) (30%, PIN; 22%, carcinoma); the remaining markers showed immunoreactivity in fewer than 5% of cases (somatostatin, calcitonin, corticotropin) or in no cases (thyrotropin, prolactin, and glucagon). At least one of the markers was present in 88% of cases of PIN and 92% of carcinoma. Non-neoplastic epithelial cells expressed serotonin, NSE, chromogranin, and hCG in every case, and the expression was significantly greater than in PIN and cancer. Stepwise regression analysis revealed the following positive correlations: chromogranin expression in PIN and patient age, NSE expression in cancer and number of lymph node metastases, and hCG expression in cancer and percentage of Gleason pattern 5; serotonin expression in PIN and cancer did not correlate with any of the clinical and pathologic factors. Neuroendocrine differentiation is downregulated in prostatic carcinogenesis, with intermediate levels of expression in PIN compared with normal cells and carcinoma.
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PMID:Neuroendocrine differentiation in prostatic intraepithelial neoplasia and adenocarcinoma. 797 47

In contrast to paraganglia of the urinary bladder, prostatic paraganglia have been largely unreported. Following the discovery of paraganglia in two separate radical prostatectomy specimens, we reviewed 100 randomly selected radical prostatectomy specimens to document the location and frequency of prostatic paraganglia. Twelve additional paraganglia were identified in eight resections, for a total of 14 paraganglia in 10 cases. Most paraganglia were located in or adjacent to lateral neurovascular bundles and, rarely, in lateral prostatic stroma. The size of paraganglia ranged from 0.1 to 1.7 mm (median 0.9 mm). Paraganglia consisted of clusters of cells in patterns that ranged from lobular to diffuse, usually with a prominent stromal vascular component. The cells contained bland oval nuclei and clear cytoplasm, which was often abundant. Occasionally, larger cells with larger nuclei were present. Immunohistochemical stains for chromogranin, neuron-specific enolase, and synaptophysin were positive; those for prostatic-specific antigen were uniformly negative. In one of our cases, histologic similarity was noted between a paraganglion and an adjacent prostatic adenocarcinoma with a "hypernephroid" pattern. Recognition of prostatic paraganglia, with appropriate immunohistochemical stains when necessary, will obviate the possibility of confusing these structures with prostatic adenocarcinoma.
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PMID:Paraganglia of the prostate. Location, frequency, and differentiation from prostatic adenocarcinoma. 814 32


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