Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0007112 (prostatic adenocarcinoma)
 2,574 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Radical prostatectomy is one treatment for organ-confined prostatic adenocarcinoma. Dissemination of malignant prostatic cells after radical prostatectomy could be partly due to prostate manipulation during dissection. We confirmed by assay of prostate-specific membrane antigen by reverse-transcription nested PCR that prostate manipulation seeded prostatic epithelial cells in the general circulation in 12 of 14 consecutive patients operated on for organ-confined prostate adenocarcinoma. Our results suggest that surgeons should approach radical prostatectomy with care to avoid seeding from the prostate gland. Antiandrogen therapy might reduce the haematogenous spread of prostatic cells during radical prostatectomy.
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PMID:Haematogenous dissemination of prostatic epithelial cells during radical prostatectomy. 862 40

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

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

The widespread use of prostate-specific antigen (PSA) has revealed that radiation therapy cures adenocarcinoma of the prostate less frequently than previously believed. Biologic factors (such as the complex nature of this disease) and technical factors (geographic miss, inadequate dose to the tumor volume) affect the ability of radiation to effectively treat all patients with prostate cancer. To improve treatment outcome, patients with virulent forms of the disease must be identified. The use of prognostic markers (PSA, prostate-specific membrane antigen, prostate-specific antigen doubling time) and genetic markers (12 lipoxygenase, p53, bcl-2, ploidy) may aid in the development of treatments for these patients. Technical modifications have been made to increase the total dose delivered to the prostate and the accuracy of dose delivery. Brachytherapy, proton therapy and conformal radiation therapy have been used to increase the relative integral dose. Improved prostate targeting may be achieved with the use of fiducial markers, on-line portal imaging, and endorectal magnetic resonance imaging. High linear energy transfer radiation, radiosensitizers and altered fractionation have been used in an attempt to increase the biologic equivalent dose to the tumor. Lastly, hormonal therapy and chemotherapy have been shown to decrease tumor burden and improve local control. All of these methods may improve outcome in patients with adenocarcinoma of the prostate. However, further work must be completed to translate these methods into standards of care.
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PMID:A rational approach to the treatment of prostate cancer with radiation therapy: lessons for the future. 942 69

Nested reverse transcription (RT)-PCR for prostate-specific antigen (PSA) and prostate-specific membrane antigen (PSM) can detect circulating prostatic cells in patients with prostate cancer. We evaluated the role of a combined screening approach for PSA and PSM in prostate cancer staging. We examined the peripheral blood samples from 136 patients with adenocarcinoma of the prostate (PCA), 15 patients with benign prostatic hyperplasia, 15 normal male subjects, and 5 female subjects. The controls (benign prostatic hyperplasias, normal males, and normal females) were negative for both PSA and PSM. In patients with metastatic PCA (n = 11), 100% were positive by combined PSA/PSM (64% by PSA and 91% by PSM). In biochemical failure PCA patients (n = 18), 39% were positive by PSM, compared to only 6% by PSA. In patients with clinically localized PCA (n = 107), 48% were positive by combined PSA/PSM approach (43% by PSM and 14% by PSA). These results show that PSM is a more sensitive marker than PSA in detecting circulating prostatic cells (P < 0.0001). We correlated preoperative RT-PCR results with final pathological stages in 67 prostatectomy patients. RT-PCR positivity was 81.5% in patients with non-organ-confined disease versus 37.5% in organ-confined disease (P = 0.001). PSA/PSM RT-PCR had an odds ratio of 7.3 (95% confidence interval, 2.3-23.4; P = 0.001) in predicting tumor extracapsular extension. PSA/PSM RT-PCR was a better predictor of tumor extracapsular extension than initial serum PSA, clinical stage, and biopsy Gleason score. Our data show that PSA/PSM nested RT-PCR may provide the staging information unavailable from the current modalities. The ultimate impact of this technique in the management of patients with prostate cancer will require continued investigation.
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PMID:Combined nested RT-PCR assay for prostate-specific antigen and prostate-specific membrane antigen in prostate cancer patients: correlation with pathological stage. 953 48

Although adenocarcinoma of the prostate is recently becoming one of most common malignancies in Japanese men, it still poses many questions regarding its etiology, pathology, pathogenesis and clinical management. Many reports have been made on oncogene and tumor suppressor gene, however, frequent genetic alterations have not been identified during prostate cancer development. Loss of heterozygosity (LOH) on 8p might be an important event in the early stage of prostatic carcinogenesis, whereas alteration in 17p is now considered a late event. Numerous reports about the androgen receptor (AR) gene have revealed that mutations in the coding region of AR possibly results in an acquired resistance to androgen blockade therapy and anti-androgen withdrawal syndrome. It has been also shown that shorter CAG repeats of AR gene are associated with a higher risk of prostate cancer. Regarding molecular diagnosis, prostate-specific membrane antigen (PSM) appears to be a new molecule with many potentially valuable applications. PSM-reverse transcriptase-polymerase chain reaction (RT-PCR) is probably more sensitive and specific than PSA-RT-PCR to predict micrometastatic disease. Gene therapy based on the above molecular aspect is currently under investigation but not generally used yet.
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PMID:[Molecular biological aspect]. 961 16

Prostate-specific membrane antigen (PSMA) is a type II integral membrane glycoprotein that was initially characterized by the monoclonal antibody (mAb) 7E11. PSMA is highly expressed in prostate secretory-acinar epithelium and prostate cancer as well as in several extraprostatic tissues. Recent evidence suggests that PSMA is also expressed in tumor-associated neovasculature. We examined the immunohistochemical characteristics of 7E11 and those of four recently developed anti-PSMA mAbs (J591, J415, and Hybritech PEQ226.5 and PM2J004.5), each of which binds a distinct epitope of PSMA. Using the streptavidin-biotin method, we evaluated these mAbs in viable prostate cancer cell lines and various fresh-frozen benign and malignant tissue specimens. In the latter, we compared the localization of the anti-PSMA mAbs to that of the anti-endothelial cell mAb CD34. With rare exceptions, all five anti-PSMA mAbs reacted strongly with the neovasculature of a wide spectrum of malignant neoplasms: conventional (clear cell) renal carcinoma (11 of 11 cases), transitional cell carcinoma of the urinary bladder (6 of 6 cases), testicular embryonal carcinoma (1 of 1 case), colonic adenocarcinoma (5 of 5 cases), neuroendocrine carcinoma (5 of 5 cases), glioblastoma multiforme (1 of 1 cases), malignant melanoma (5 of 5 cases), pancreatic duct carcinoma (4 of 4 cases), non-small cell lung carcinoma (5 of 5 cases), soft tissue sarcoma (5 of 6 cases), breast carcinoma (5 of 6 cases), and prostatic adenocarcinoma (2 of 12 cases). Localization of the anti-PSMA mAbs to tumor-associated neovasculature was confirmed by CD34 immunohistochemistry in sequential tissue sections. Normal vascular endothelium in non-cancer-bearing tissue was consistently PSMA negative. The anti-PSMA mAbs reacted with the neoplastic cells of prostatic adenocarcinoma (12 of 12 cases) but not with the neoplastic cells of any other tumor type, including those of benign and malignant vascular tumors (0 of 3 hemangiomas, 0 of 1 hemangioendothelioma, and 0 of 1 angiosarcoma). The mAbs to the extracellular PSMA domain (J591, J415, and Hybritech PEQ226.5) bound viable prostate cancer cells (LNCaP and PC3-PIP), whereas the mAbs to the intracellular domain (7E11 and Hybritech PM2J004.5) did not. All five anti-PSMA mAbs reacted with fresh-frozen benign prostate secretory-acinar epithelium (28 of 28 cases), duodenal columnar (brush border) epithelium (11 of 11 cases), proximal renal tubular epithelium (5 of 5 cases), colonic ganglion cells (1 of 12 cases), and benign breast epithelium (8 of 8 cases). A subset of skeletal muscle cells was positive with 7E11 (7 of 7 cases) and negative with the other four anti-PSMA mAbs. PSMA was consistently expressed in the neovasculature of a wide variety of malignant neoplasms and may be an effective target for mAb-based antineovasculature therapy.
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PMID:Five different anti-prostate-specific membrane antigen (PSMA) antibodies confirm PSMA expression in tumor-associated neovasculature. 1039 65

Prostatic small cell carcinoma is an aggressive subtype of prostate cancer that usually appears as a progression of the original adenocarcinoma. We describe here the WISH-PC2, a novel neuroendocrine xenograft of small cell carcinoma of the prostate. This xenograft was established from a poorly differentiated prostate adenocarcinoma and is serially transplanted in immune-compromised mice where it grows within the prostate, liver, and bone, inducing osteolytic lesions with foci of osteoblastic activity. It secretes to the mouse Chromogranin A and expresses prostate plasma carcinoma tumor antigen-1, six-transmembrane epithelial antigen of the prostate, and members of the Erb-B receptor family. It does not express prostate-specific antigen, prostate stem cell antigen, prostate-specific membrane antigen, and androgen receptor, and it grows independently of androgen. Altogether, WISH-PC2 provides an unlimited source in which to study the involvement of neuroendocrine cells in the progression of prostatic adenocarcinoma and can serve as a novel model for the testing of new therapeutic strategies for prostatic small cell carcinoma.
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PMID:WISH-PC2: a unique xenograft model of human prostatic small cell carcinoma. 1111 33

The current approach to prostate cancer diagnosis has major limitations including the inability of prostate-specific antigen (PSA) assays to accurately differentiate between prostate cancer and benign prostate hyperplasia (BPH) and the imprecision of transrectal ultrasound (TRUS) biopsy sampling. We have employed cDNA microarray screening to compare gene expression patterns in BPH and tumour samples to identify expression markers that may be useful in discriminating between these conditions. Screening of 3 individual cDNA arrays identified 8 genes with expression 3-fold greater in 6 tumour tissues than in 1 nontumour sample and 1 BPH sample. Real-time PCR was used to confirm the overexpression of these 8 genes and 12 genes selected from the literature against a panel of 17 tumours and 11 BPH samples. Two genes, delta-catenin (delta-catenin; CTNND2) and prostate-specific membrane antigen (PSMA; FOLH1), were significantly overexpressed in prostate cancer compared to BPH. Prostate epithelial cells stained positively for delta-catenin and PSMA in our prostate cancer tissues, whereas the majority of our BPH tissues were negative for both markers. Thus we have identified delta-catenin (not previously associated with prostatic adenocarcinoma) and confirmed the potential of PSMA as potential candidates for the diagnosis and management of prostate cancer.
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PMID:Expression analysis of delta-catenin and prostate-specific membrane antigen: their potential as diagnostic markers for prostate cancer. 1211 74

Small cell carcinoma of prostate is rare, with the literature consisting of case reports and small series. The current work analyzes the morphology and immunohistochemistry of 95 cases of prostatic small cell carcinoma diagnosed at our institution. Specimens included 55 needle biopsies, 27 transurethral resections, 4 radical prostatectomies, and 9 biopsies from metastatic sites (some patients with >1 procedure). Patients ranged in age from 44 to 92 years old (mean: 69 y). Although serum prostate-specific antigen (PSA) in some cases was very high (up to 1896 ng/mL), the median value was only 4.0 ng/mL. Of cases with available information, 33/78 (42%) had a history of usual prostatic adenocarcinoma. The interval between the diagnosis of small cell carcinoma and prior usual prostatic cancer ranged from 1 to 300 months (median 25 mo). Pure small cell carcinoma was seen in 54/95 (57%) of cases with the remaining cases admixed with prostate adenocarcinoma. In cases with adenocarcinoma, there was a sharp demarcation between small cell carcinoma and adenocarcinoma in 20.5% of cases; in the remaining cases there was gradual merging of the 2 components. In mixed cases, small cell carcinoma predominated (median: 80% of the tumor); the Gleason score of the adenocarcinoma was > or =8 in 85% of these cases. In 61 cases (64%), small cell carcinoma was classic "oat cell" morphology with remaining the "intermediate cell" variant. Of the 95 cases: necrosis was seen in 40% (2% to 95% of the tumor); giant bizarre cells in 19%; Indian filing in 21%; rosette formation in 29%; focal vacuolated cytoplasm in 18%; and desmoplasia in 20%. Most (88%) of small cell carcinoma were positive for at least 1 neuroendocrine marker. In the small cell carcinoma component, 14/73 (19%) were positive for PSA, 17/61 (28%) positive for prostein (P501S), and 15/59 (25%) positive for prostate-specific membrane antigen, although often very focally. Stains for thyroid transcription factor-1 were positive in 23/44 (52.3%) cases. In this, the largest study of prostatic small cell carcinoma, we highlight the presence of morphologic features that may result in its underdiagnosis. Other more classic histologic features of small cell carcinoma along with rosettes are critical for its accurate diagnosis. P501S and prostate-specific membrane antigen were better in identifying the prostatic origin of small cell carcinoma than PSA, although the majority (60%) of prostatic small cell carcinomas were negative for all 3 markers.
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PMID:Small cell carcinoma of the prostate. A morphologic and immunohistochemical study of 95 cases. 1816 72


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