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Query: UMLS:C0600139 (Prostate Cancer)
 4,540 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recent epidemiologic studies have suggested that a risk factor for the development of carcinoma of the prostate may be previous vasectomy. As a majority of prostate cancer cases diagnosed in the U.S. are detected by an elevation in prostate-specific antigen (PSA), an elevation in PSA due to vasectomy may underpin this association. There have been no published reports on the relationship between PSA before and after vasectomy. To study this relationship, this study was undertaken to determine the effects of vasectomy on PSA. Twenty-five men undergoing vasectomy were studied with serial PSA determinations prior to and following vasectomy. Analysis of data suggests that PSA is not affected by previous vasectomy and that other causes for an increased detection in this cohort may be operational.
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PMID:Serum prostate-specific antigen concentration before and after vasectomy. 870 Mar 33

Serum prostate-specific antigen (PSA) has greatly enhanced our ability to detect carcinoma of the prostate. Yet, because of its lack of specificity for malignancy, approximately two thirds of the men with an elevated PSA level do not have prostate cancer. This problem is particularly relevant to men whose prostate feels normal by digital rectal examination (DRE) and appears normal by transrectal ultrasound (TRUS). Carcinoma of the prostate, if detected in these men, is staged as T1c and is usually considered to be of clinical significance. Attempts at refining PSA have included attempts to correct the serum level relative to the size of the prostate (PSA density). Although conflicting data has been reported in the literature, it appears when stratified for PSA ranges between 4 and 10 ng/mL, PSA density does not provide an advantage over PSA alone in cancer detection in patients with a normal DRE and TRUS.
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PMID:Use of prostate-specific antigen (PSA) and PSA density in the detection of stage T1 carcinoma of the prostate. 886 74

Digital rectal examination, prostate-specific antigen and transrectal sonography (TRS) are the main diagnostic tools for evaluating men at risk for carcinoma of the prostate (PCa). PCa has a hypoechoic echo pattern via TRS in 60- 85% of cases. Hypoechoic areas are observed, however, in benign prostatic hyperplasia (BPH) as well. For this reason, TRS yields a low specificity and sensitivity in detecting PCa in screening programs. Additional data, independent of the grey scale information available via TRS, can be obtained by using the innovative technology of color Doppler sonography. This imaging modality allows simultaneous real-time sonographic visualization and evaluation of vascular structures. The present study analyzes to what extent the analysis of blood flow perfusion of prostatic parenchyma can provide further information concerning the pathologic alterations occurring in abnormal prostate tissue. Blood flow phenomena were reproducibly demonstrated in the prostate and in the periprostatic tissue with the color-coded Doppler sonography (CD-TRS). 31 patients with the diagnosis of BPH could be separated into two different groups according to the findings with TRS and CD-TRS. In contrast, patients with histologically proven PCa (n = 16) had subjectively increased perfusion rates. Blood flow phenomena were analyzed using computer-calculated resistive index and pulsatility index as evaluations of flow and frequency. A preliminary analysis of the wave-form characteristics shows that flow in the prostate gland is associated with a high resistive index in both PCa and BPH. The mean frequency demonstrated in the pulsatility index appears to be high in PCa, but low in BPH cases. Further studies are needed to verify the described factors' abilities to differentiate prostate tissue as either PCa or BPH.
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PMID:Color Doppler sonography of the prostate. 891 44

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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PMID:Two cases of small cell carcinoma of the prostate. 900 36

In this communication a limited analytical study is described on the new Prostatus PSA Free/Total assay. The study is considered as a side study of the European Randomized Study of Screening for Prostate Cancer. The between-day imprecision with 8 control samples for free prostate-specific antigen ranged from 10.3% at 0.17 microg/l to 3.7% at a concentration of 35.5 microg/l, while for total prostate-specific antigen we found 7.3% at 0.69 microg/l and 4.3% at 70.7 microg/l. For total prostate-specific antigen we found excellent agreement between the new assay and well-established assays like Abbott IMx and Hybritech Tandem-E, both for prostate cancer and benign prostate hyperplasia specimens. The age-specific reference ranges proved to be well-comparable with the literature data both for free and total prostate-specific antigen.
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PMID:Analytical evaluation of the new Prostatus PSA Free/Total assay for prostate-specific antigen as part of a screening study for prostate cancer. 905 53

Primary prostatic duct adenocarcinoma, initially labeled as endometrioid carcinoma of the prostate, is a rare neoplasm that displays exophytic growth into the prostatic urethra with involvement of prostatic ducts. Because this tumour arises from preexisting epithelia, there is a possibility that a remnant basal epithelium may be seen in association with these tumours. If this hypothesis is correct, then prostatic duct adenocarcinoma may possibly be mistaken for high-grade prostatic intraepithelial neoplasia (PIN) on needle biopsies. The distribution of basal cells in this tumour has not been described previously. Nine cases of prostatic duct adenocarcinoma and prostatic adenocarcinoma with focal ductal differentiation were studied immunohistochemically with antibodies specifying cytokeratin 34 beta E12, prostate-specific antigen (PSA), and prostatic acid phosphatase (PAP). All cases were positive for PSA and PAP. In some areas of the tumour in eight cases there was a continuous and discontinuous layer of basal cells surrounding islands of carcinoma. This was found with cribriform, comedo, solid, and papillary components of ductal type adenocarcinoma. It is necessary to be aware of the presence of basal cells in association with primary prostatic duct adenocarcinoma. Differentiation of high-grade PIN from this lesion should depend on complex architectural characteristics and Cytologic features rather than presence of a basal cell layer. This finding confirms that the solid, cribriform, papillary, and comedo components initially grow intraluminally within ducts before invasion into surrounding stroma occurs.
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PMID:Distribution pattern of basal cells detected by cytokeratin 34 beta E12 in primary prostatic duct adenocarcinoma. 913 Sep 90

At present, only locally confined carcinoma of the prostate can be cured if all of the tumor tissue can be removed by surgery [36]. Early detection strategies using serum prostate-specific antigen (PSA), digital rectal examination (DRE) and transrectal ultrasound (TRUS) have been increasingly used. However, exact clinical determination of the local tumor extension is only possible to a limited extent [4, 13, 28, 34]. Up to 60% of clinical locally confined tumors are understaged after histopathological examination of the radical prostatectomy specimen. Furthermore a high incidence of positive margins of up to 60% has been reported [7, 21]. Although a clear surgical margin does not exclude local or distant disease recurrence, it is regarded as a good prognostic factor [3, 25]. Androgen withdrawal prior to radical prostatectomy is an attractive theoretical option to decrease the risk of disease recurrence, since tumor regression can be induced by any procedure that reduces the intracellular concentration of dihydrotesterone by more than 80%. The benefit of preoperative medical androgen deprivation is controversial [6-8, 13, 15-17, 20, 23, 35, 37]. A priori a benefit would not be expected in any case if androgen withdrawal had no effect on the tumor. We therefore investigated the effects of a neo-adjuvant androgen-ablative therapy (NAT) in a large population of 375 patients who underwent radical retropubic prostatectomy (RRP) after NAT. We report in particular the effects of NAT on prostate volume measured by TRUS, PSA, clinical stage and tumor morphology including positive surgical margins. Furthermore the recently reported first results of prospective randomized trials comparing RRP alone versus NAT plus RRP are discussed to analyze the possible impact of NAT.
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PMID:Neo-adjuvant hormonal therapy of prostate cancer. 914 88

To establish normal reference values for prostate-specific antigen (PSA) in a Swedish population we investigated 878 healthy men, 56-75 years of age. They were randomly selected from a population of 9171 males in this group. Cancer of the prostate was excluded by digital rectal examination. When digital rectal examination was suspicious for carcinoma of the prostate and/or serum PSA > 4 micrograms l-1, fine-needle aspiration biopsy was performed. Central values, values of variance and reference limits were defined by a non-parametric method in four age groups. A strong positive correlation between PSA values and age was found and the variance increased with age. The relationship between PSA value and age was non-linear. For the age group 56-60 the upper reference limit (95th percentile) was 4.6 micrograms l-1 (confidence interval, CI: 3.9-5.5). For the age groups 61-65, 66-70 and 71-75 the corresponding values were 4.4 (3.8-5.2), 7.6 (6.5-8.9) and 8.4 micrograms l-1 (7.2-9.8) respectively. For the age groups studied the increment over time of the PSA value was 2-8% per year depending on age, with an average increment per year over 15 years of 4.3%. Overall, 11% of our reference sample had a serum PSA level > 4 micrograms l-1. We consider our study population to be representative for a normal Swedish male population in these age groups.
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PMID:Age-specific reference values for serum prostate-specific antigen in a community-based population of healthy Swedish men. 923 58

High-grade prostatic intraepithelial neoplasia (HGPIN) is the most likely precursor proliferation of peripheral zone, moderately to poorly differentiated prostatic adenocarcinomas. The usual cell type of the epithelial lining of HGPIN is a glandular epithelial cell with characteristic nuclear abnormalities. Here we report nine cases of unusual types of HGPIN, including three cases of signet-ring cell HGPIN, one case of small cell neuroendocrine HGPIN, and five cases of HGPIN with distinctive mucinous features. The three examples of signet-ring cell PIN were all associated with an invasive primary signet-ring cell carcinoma of the prostate. The HGPIN assumed a classical tufted and micropapillary architectural growth pattern, with the constituent cells exhibiting a morphologic appearance identical to that of the invasive signet-ring cells. The intraepithelial and invasive signet-ring cells were mucin negative and were immunoreactive for prostate-specific antigen (PSA). A fourth case displayed a mixed intraepithelial glandular-small cell neoplastic proliferation, where intraepithelial small cells were histologically identical to surrounding invasive small cell carcinoma cells. The small cell HGPIN and invasive small cell carcinoma cells were positive for the neuroendocrine markers chromogranin, synaptophysin, and neuron-specific enolase. In five cases, mucinous distension of HGPIN glands, producing a flat pattern of the epithelial lining layer, comprised the third unusual pattern of HGPIN. These blue mucinous secretions were readily detected by hematoxylin and eosin staining and were composed of both neutral (periodic acid-Schiff-positive) and acidic (alcian blue-positive) mucins. Herein we document the existence of an intraepithelial proliferation of neoplastic cell types-small cell neuroendocrine and signet-ring cell-that are usually considered as stromal-invasive cells in the prostate. The presence of these rare prostatic cell types in both HGPIN and invasive carcinoma provides further support for a close relationship between HGPIN and invasive carcinoma of the prostate. All three unusual types of HGPIN-signet-ring cell, small cell neuroendocrine, and mucinous-are important to diagnostically recognize because of the strength of association of HGPIN with invasive carcinoma.
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PMID:Unusual histologic types of high-grade prostatic intraepithelial neoplasia. 933 Dec 95

Our laboratory has developed two cellular models of human prostate cancer progression. The LNCaP prostate cancer progression model is based upon the well-known cellular interaction between human prostate or bone stromal cells and LNCaP cells in vivo. The marginally tumorigenic LNCaP cells acquired tumorigenic and metastatic potential upon cellular interaction with either prostate or bone fibroblasts. A subline termed C4-2 was observed to grow readily in castrated animals and acquired metastatic potential spreading from the primary tumor site to the lymph node, the seminal vesicles, and the axial skeleton, resulting in an intense osteoblastic reaction. The second model is ARCaP, where prostate cancer cells derived from the ascites fluid of a man with metastatic disease exhibited an Androgen- and estrogen-Repressed Prostate Cancer cell growth and tumor formation in either a hormone-deficient or a castrated environment. However, the growth of either the tumor cells in vitro or the tumors in vivo was suppressed by both estrogen and androgen. While the tumor cells expressed low levels of androgen receptor and prostate-specific antigen (PSA), they were highly metastatic when inoculated orthotopically. Distant metastases to a number of organs were detected, including the liver, lung, kidney, and bone. We have employed a human prostate cancer progression model as a system to study the efficacy of gene therapy. Results of the study show that whereas universal promoters, such as Cytomegalovirus (CMV) and Rous Sarcoma Virus (RSV) promoter-driven tumor suppressors (e.g. p53, p21, and p16), were effective in inhibiting prostate tumor growth, the advantages of driving the expression of therapeutic toxic genes using a tissue-specific promoter prostate-specific antigen (PSA) and a tumor--but not tissue-specific promoter, osteocalcin (OC), are preferred. In the case of the PSA promoter, we can achieve cell-kill in PSA-producing human prostate cancer cells. To circumvent the supporting role of bone stroma for prostate cancer epithelial growth, we have recently developed a novel concept where the expression of therapeutic toxic genes is driven by a tumor--but not a tissue-specific OC promoter. Osteocalcin-thymidine kinase (OC-TK) was found to efficiently eradicate the growth of osteosarcoma, prostate, and brain tumors both in vitro and in vivo. We observed that androgen-independent human prostate cancer cells lines expressed OC-TK at higher levels than androgen-dependent human prostate cancer cell lines. We have obtained data to suggest that Ad-OC-TK plus a pro-drug acyclovir (ACV) may be used as an effective therapy to treat prostate cancer bone metastasis in models where the growth of androgen-independent PC-3 and C4-2 tumors in the bone has occurred.
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PMID:Human prostate cancer progression models and therapeutic intervention. 943 28


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