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

We describe a 67-year-old man with a history of Stage B1 adenocarcinoma of the prostate who was treated with iodine-125 implantation in 1985. His prostate-specific antigen values subsequently increased in conjunction with an intraprostatic recurrence. Biopsy revealed primary squamous cell carcinoma arising in the prostate; no adenocarcinomatous elements were noted.
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PMID:Primary squamous cell carcinoma of the prostate after radiation seed implantation for adenocarcinoma. 754 81

Previous studies have suggested that serum prostate-specific antigen (PSA) levels are under androgenic influence, especially in patients with adenocarcinoma of the prostate. PSMA (prostate-specific membrane antigen) is thought to reflect hormonal or clonal resistance or an independence with respect to testosterone regulation. The influence of testosterone on serum PSA expression in normal men is not clear. We studied the effect of exogenous testosterone administration on the serum levels of PSA and PSMA in hypogonadal men. Serial serum PSA, serum PSMA by Western blot, and serum total testosterone levels were obtained at intervals of every 2-4 weeks in 10 hypogonadal men undergoing treatment with exogenous testosterone, delivered as testosterone enanthate injection or by testosterone patch. Linear and quadratic orthogonal polynomial scores were calculated for PSMA, PSA, and testosterone. A 2-tailed, paired t-test failed to demonstrate a significant correlation between serum PSA (linear P = 0.432, quadratic P = 0.290) or PSMA (linear P = 0.162, quadratic P = 0.973) and serum testosterone levels. This study suggests that in hypogonadal men, neither PSMA nor PSA expression is testosterone-dependent.
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PMID:Effect of exogenous testosterone replacement on prostate-specific antigen and prostate-specific membrane antigen levels in hypogonadal men. 754 73

Serum and seminal plasma concentrations or activities of acid phosphatase (AP), prostate specific antigen (PSA), and canine prostate specific esterase (CPSE) were measured in normal dogs, dogs with benign prostatic hyperplasia (BPH), dogs with bacterial prostatitis, and dogs with prostatic carcinoma to determine if these assays would be of value in differentiating dogs with prostatic carcinoma from normal dogs, and dogs with other prostatic disorders. In addition, tissue sections of prostatic adenocarcinomas were stained with antiprostatic AP, anti-CPSE, and anti-PSA antibodies to determine if these would be suitable immunohistochemical markers of prostatic carcinoma. Prostate-specific antigen was not detected in canine serum or seminal plasma. Serum and seminal AP activities did not differ significantly between normal dogs and those with prostatic diseases, or among dogs with different prostatic disorders. Serum CPSE activities were significantly higher in dogs with BPH than in normal dogs. Mean serum CPSE activities in dogs with BPH, bacterial prostatitis, and prostatic carcinoma were not significantly different from each other. Slight to moderate immunohistochemical staining of canine prostatic adenocarcinomas was noted for prostatic AP and PSA; most tumors did not stain for CPSE. These results show that proteins of prostatic origin appear in the serum of dogs as a result of prostatic pathology, especially BPH. Canine prostatic adenocarcinoma does not appear to be associated with significant increases in CPSE or AP activities, possibly because of down-regulation of these enzymes by prostatic carcinoma cells. It is also possible that failure to detect significant differences resulted from limited statistical power for some groups and pairwise analyses because of the small number of dogs evaluated.
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PMID:Evaluation of serum and seminal plasma markers in the diagnosis of canine prostatic disorders. 754 54

Two cases of florid hyperplasia of mesonephric remnants occurring in the prostate are described. One case was originally interpreted as invasive adenocarcinoma on transurethral resection (TUR), resulting in radical prostatectomy. In the second case, a TUR specimen was diagnostic for adenocarcinoma, which was confirmed in the radical prostatectomy specimen. Florid mesonephric hyperplasia in the second case was an incidental finding. The TUR specimen in the first case and sections of the prostatectomy specimens in both cases contained a proliferation of tubules, which ranged from aggregates of microacini to dilated structures containing a characteristic colloid-like material. The location of these lesions in the base of the prostate gland and periprostatic soft tissue suggests that these may be mesonephric remnants that have become hyperplastic. This type of lesion shares many features with mesonephric hyperplasia occurring in the female genital tract, including the presence of eosinophilic intratubular material and a lobular arrangement of microacini lined by a single layer of epithelium with prominent nucleoli. However, the latter feature, along with the apparent permeation of the prostatic fibromuscular stroma, periprostatic soft tissue, and even neural spaces, closely mimicked prostatic adenocarcinoma. In both cases, the proliferating tubules reacted with keratin 903 and were negative for prostate-specific antigen and prostate acid phosphatase, thereby excluding the diagnosis of prostatic adenocarcinoma. We concluded that lobular hyperplasia of mesonephric remnants is a distinct histologic entity that may occur in the prostate and periprostatic soft tissues and closely mimic prostatic adenocarcinoma.
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PMID:Florid hyperplasia of mesonephric remnants involving prostate and periprostatic tissue. Possible confusion with adenocarcinoma. 768 79

The tissues consisted of adenocarcinoma of the prostate were examined by immunohistochemical study with monoclonal antibody (43-21-1-1) against gamma-seminoprotein (gamma Sm)2). The degree of staining regarding any correlation with the histological grade was evaluated. The prostatic tissues were obtained by transurethral resection or by fine needle biopsy from untreated 38 patients. The avidin-biotin peroxidase complex technique was used to stain on 3 microns-sections of 10% formalin fixed, paraffin embedded tissue. In addition, immunohistochemical staining with the commercialized antibodies to prostate-specific antigen (PSA; polyclonal, DAKO) and to prostatic acid phosphatase (PAP; polyclonal, DAKO) was done simultaneously for a comparative study. The degree of immunoperoxidase stain was classified into two categories, namely location and pattern, and was graded from 0 to 3, respectively. The product of the degree of location and the degree of pattern was noted as the total score. The mean of score was calculated in each histological grade. Then the means of total scores were compared and evaluated as having any statistical difference by Student's t test among 3 histological grades as well as among 3 primary antibodies used in this study. When the monoclonal antibody to gamma-Sm was used for immunoperoxidase staining, the means of total scores and the rates of negative reactions (% Negative) in 3 histological grades were 6.8 +/- 1.8 (M +/- SD) and 0% in well (N = 9), 4.4 +/- 2.4 and 14% in moderately (N = 22), and 1.8 +/- 2.3 and 54% in poorly differentiated lesions (N = 11), respectively. There were statistically significant differences (P < 0.05) among 3 histological grades.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Immunohistochemical study of monoclonal antibody against gamma-seminoprotein in the prostatic tissues. A significant correlation between the degree of staining and the histological grade of adenocarcinoma of the prostate]. 768 1

We studied 33 cases with an initial needle biopsy of the prostate that showed only high-grade prostatic intraepithelial neoplasia (PIN 2-3), for which follow-up biopsies were available. Twenty-four men (73%) were shown to have adenocarcinoma either on a simultaneous (14 patients) or subsequent (10 patients) biopsy. The grade of PIN (grade 2 v 3), rectal examination findings, and transrectal ultrasound results proved not to be significantly different in patients with proven adenocarcinoma compared with those without proven carcinoma. In contrast, serum prostate-specific antigen (PSA) concentrations were elevated in 90% of patients with carcinoma compared with only 50% of those with a benign follow-up biopsy. Persistent elevation of serum PSA concentration was seen in only one of three patients with serial PSA measurements and a benign follow-up biopsy. Notably, all patients with carcinoma for whom we had serial measurements of serum PSA levels had persistent elevation. The finding of high-grade PIN on needle biopsy often represents a sampling problem with carcinoma nearby. Consequently, the finding of high-grade PIN on needle biopsy merits vigorous follow-up, including rebiopsy. In particular, patients with increased serum PSA appear to be at greater risk of harboring prostatic adenocarcinoma. However, a significant number of patients with high-grade PIN on initial biopsy may not have evidence of carcinoma on repeat biopsy. Thus, radical prostatectomy or radiotherapy for PIN is not warranted.
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PMID:Significance of high-grade prostatic intraepithelial neoplasia on needle biopsy. 768 99

We report a rare case of primary signet ring cell adenocarcinoma of the prostate in a 61-year-old male, who died of systemic lymphatic spread. Autopsy ruled out another primary signet ring cell adenocarcinoma outside the prostate. However, immunohistochemically, the tumor stained negatively for prostate-specific antigen. A review of the literature revealed only 15 case reports, including our case.
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PMID:Primary signet ring cell adenocarcinoma of the prostate: a case report and literature review. 768 15

We describe a patient with adenosquamous carcinoma of the prostate. His history suggests a common histogenesis of the glandular and squamous elements of the tumor. A 60-year-old white man had adenocarcinoma of the prostate diagnosed by biopsy and then underwent radical prostatectomy, which showed adenosquamous carcinoma. Immunoperoxidase in the glandular component was positive for prostate-specific antigen (PSA), prostatic acid phosphatase (PAP), and low molecular weight keratin CAM 5.2 but was negative for high molecular weight keratin AE-3. The squamous component was negative for PSA, PAP, and CAM 5.2 but positive for AE-3. Previously reported patients with adenosquamous carcinoma of the prostate share a history of radiation or hormonal therapy followed much later by prostatectomy, suggesting that adenosquamous carcinoma consists of residual primary adenocarcinoma and metaplastic squamous epithelium caused by radiation or hormonal treatment. However, the present case lacks this history, suggesting that the two types of epithelia may have developed concurrently.
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PMID:Adenosquamous carcinoma of the prostate. 782 10

Recent studies have demonstrated that retinoic acid (RA) can repress the growth of human prostatic epithelial cells. Since the proliferation of prostate cells is highly dependent on androgen stimulation, presumably via its cognate receptor, we investigated the effects of RA on the expression of the androgen receptor and other androgen-regulated genes in the human prostatic adenocarcinoma cell line LNCaP. Using a radioligand binding assay, we found that androgen-binding activity was reduced 30-40% in cells treated with 10(-5) M RA plus 6 nM dihydrotestosterone (DHT), as compared to cells with the androgen alone. Moreover, the reduction of the androgen receptor (AR) was not accompanied by alteration of the ligand-binding affinity. Concomitant changes in the function of AR were manifested by a dramatic reduction in AR-mediated transcription activity in a transfection experiment. Androgen-induced levels of both prostate-specific antigen (PSA) and human glandular kallikrein-1 (hKLK2) mRNAs were significantly repressed by RA in a dose- and time-dependent manner. Consistent with this finding, androgen induction of PSA glycoprotein was also repressed by RA, with maximal inhibition occurring at 10(-5) M. These data suggest that the suppression of proliferation and function of prostatic cells by RA may be via modulatory effects on the AR.
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PMID:Antagonism of androgen action in prostate tumor cells by retinoic acid. 802 10

There is a need for the development of new diagnostic tools for the early detection of prostate cancer. A candidate molecule for a new screening test is a prostate-specific membrane antigen (PSM) recognized by the monoclonal antibody 7E11.C5. We carried out studies aimed at identifying PSM in the serum of normal and benign prostatic hyperplasia (BPH) donors and patients with adenocarcinoma of the prostate, in order to judge whether the development of a serum assay using this marker was feasible. By Western blotting, we found significant levels of PSM in serum samples from prostatic cancer patients, in the seminal fluid of pooled normal donors, in BPH patients, and in normal male sera. Similar to prostate-specific antigen (PSA), PSM was present in seminal plasma in higher concentrations than in serum, and PSM levels in prostatic cancer patients were significantly higher than in normal controls. These data suggest that the development of an assay utilizing the PSM and new monoclonal antibodies directed against the antigen, could provide a feasible test for prostatic cancers.
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PMID:Western blot assay for prostate-specific membrane antigen in serum of prostate cancer patients. 808 37


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