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Query: UMLS:C0376358 (prostate cancer)
 59,338 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two morphologically different types of intracisternal virus-like particles were observed electron microscopically in a biopsy specimen of human prostate cancer. Particles of one type were 150-200 nm in diameter and contained either an electron-dense core or two concentric inner layers. Particles of the other type were smaller, 80-100 nm in diameter, and appeared mostly in filamentous or chainlike formation. Both types of particles and budding were observed in endoplasmic cavities of epithelial tumor cells. The particles had ultrastructural characteristics that suggested a viral nature but were different from the known type B, type C, or type H (hamster type R) virus particles. This was the first election microscopic observation in prostate cancer of virus-like particles similar to those previously reported in a case of human breast carcinoma.
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PMID:Virus-like particles in a case of human prostate carcinoma. 85 30

Prostate cancer is the most commonly diagnosed form of malignant neoplasia in men. Considerable evidence has accumulated suggesting that paracrine interactions between stromal cells and epithelial cells mediate, in part, the growth and development of the prostate. A nerve growth factor-like protein secreted by stromal cells has been implicated in the paracrine regulation of prostate epithelial tumor cell growth in vitro. This prostate-derived nerve growth factor-like protein differs from the known members of the neurotrophin family of proteins, and may represent a prostate-specific form of this family of gene products. Furthermore, corresponding nerve growth factor receptors have been localized to the epithelial cells of the human prostate in vivo, consistent with a role of the receptors and the adjacent nerve growth factor-like protein secreted by stromal cells, in the paracrine regulation of prostate growth and neoplasia.
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PMID:Role of nerve growth factor-like protein in the paracrine regulation of prostate growth. 129 29

Transforming growth factor beta (TGF beta) exerts a wide spectrum of activity on many different cell types. Since TGF beta inhibits the growth of a variety of epithelial tumor cells in vitro, we examined the effects of TGF beta on the human prostate cancer cell lines DU145, PC3 and LNCaP for possible inhibitory activity. Growth in monolayer was initially inhibited in a dose-response fashion in the two androgen-independent cell lines, PC3 and DU145 but not in the androgen-dependent LNCaP cells. The rate of growth of the PC3 and DU145 cells treated with TGF beta, however, eventually returned to control levels despite retreatment with TGF beta. Anchorage-independent growth was inhibited to 55% and 16% control levels in PC3 and DU145, respectively. Scatchard analysis showed 1500 and 2900 TGF beta binding sites/cell on DU145 and PC3 cells with Kd = 6.9 and 12 x 10(-12) M, respectively. High-affinity binding could not be demonstrated on LNCaP cells. We also explored the possibility that TGF beta was secreted by these cells. Analysis of conditioned media by immunoprecipitation and a radioreceptor assay showed secretion of TGF beta into the media by DU145 and PC3 but not by LNCaP. Northern analysis showed the presence of TGF beta mRNA in DU145 and PC3, but not in LNCaP. These data indicate that TGF beta might serve as an autocrine inhibitory factor in prostate cancer. In addition, because TGF beta affects a wide range of cell types, TGF beta production by prostate cancer cells may contribute an important paracrine function in the development of tumor stromal tissue and metastases.
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PMID:Differential effects of transforming growth factor beta on human prostate cancer cells in vitro. 254 87

Overall bone metastasis (BM) was found upon autopsy in 271 (26.0%) of 1041 patients who died due to malignant epithelial neoplasm at our hospital over the last 20 years. The incidences of BM from primary organs were as follows; 71.4% for breast cancer, 70.0% for prostate, 49.6% for lung and 22.5% for stomach. The distribution of skeletal metastases was the lumber spine in 63.8% of cases, sternum in 38.0% and ribs in 26.2% as revealed by routine autopsy examination. The most common pathway of BM was the transpulmonary route, followed by the vertebral venous system which is known to be involved in metastasis to the spine. The frequency of BM via the vertebral venous system without pulmonary metastasis was 30% for carcinoma of the prostate, 10.4% for the uterus, 7.4% for the breast and 3.5% for the stomach in our examination series. Types of focal reaction to BM were classified as osteoplastic (OP), osteolytic (OL), intertrabecular and mixed types. The mixed type showed transitional and mixed features between OP and OL types. Therefore they were considered to be closely related. Relationships between primary organs and histologic appearances revealed a degree of specificity for BM. Squamous cell carcinoma in various organs and small cell carcinoma of the lung appeared to produce an OL but not OP reaction. OP was especially characteristic of prostatic cancer, poorly differentiated adenocarcinoma of the stomach and breast, in young patients. There appeared to be a relation between clinical course and the form of treatment for metastatic bone reaction.
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PMID:[Histopathology of metastatic bone tumors]. 359 9

Tissue polypeptide specific antigen (TPS) is a new tumor proliferation serotest marker. The respective radioimmunodetective procedure is based on the application of monoclonal antibodies raised against one the principle epitopes of tissue polypeptide antigen (TPA). TPS is useful tool for the identification of proliferative epithelial cells and is negative in all non-epithelial tissues such as lymph nodes, bone marrow, carcino-sarcomic and neuroendocrine prostatic tumors. In previous studies we have shown the clinical usefulness of this serotest in serial measurements during prostate cancer monitoring. In this study serum prostatic specific antigen (PSA) concentrations and natural killer (NK) cell activity data were compared with serum TPS values in a wide spectrum of prostate cancer condition (99 patients), benign prostatic hypertrophy (BPH, 40 patients), atypical prostate (12 subjects) and in 8 healthy men. Measured parameters reflect different aspects of the disease. Blood PSA concentrations and TPS serotest values were found to denote the status of disseminated prostate cancer with nearly equal significance, while PSA appears to be a more appropriate tumor marker in early stages of the disease. In atypical prostate a nonsignificant elevation of both PSA and TPA values were recorded when compared with BPH. In parallel, a pronounced and sharp drop in NK activity data was assessed resembling closely respective data in progressive Stage D2 patients. TPS serotest clearly detects cancer progression in treated and untreated patients (P < 0.01) while being less efficient in distinguishing between tumor stabilization and partial remission (p > 0.05). In this respect NK activity data serve as a sensitive probe for the presence of epithelial tumor cells in the circulation even during stabilization of the disease. According to the reported results we advocate the application of the TPS serotest as a useful addition in monitoring progressive patients with advanced prostatic carcinoma.
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PMID:Correlation of cell proliferation marker (TPS), natural killer (NK) activity and tumor load serotest (PSA) in untreated and treated prostatic tumors. 768

Detection of micrometastatic tumor cells in bone marrow of cancer patients has been shown to be of prognostic significance. To further characterize these cells, we combined antibody labeling and fluorescence in situ hybridization (FISH). For detection of numerical changes of chromosome 17, nine patients with proven breast cancer whose bone marrow contained epithelial tumor cells were evaluated. Epithelial cells were stained by anticytokeratin antibody. Afterwards FISH was performed using an alpha-satellite probe specific for chromosome 17. In a second series bone marrow epithelial cells of eight patients with breast cancer and of six with prostatic cancer were evaluated for the amplification of HER-2/neu by using a gene-specific DNA probe. In the first series four patients had only single epithelial cells in their bone marrow. Only one single cell showed five hybridization signals, whereas all other single cells showed two or less. Five patients had clusters of epithelial cells in bone marrow with or without additional single cells. One hundred four cells had three or more hybridization signals and 103 of these polysomic cells were located in tumor cell clusters. In the second series we could detect HER-2/neu amplification in bone marrow epithelial tumor cells in two of eight patients with breast cancer but in none of the prostatic cancer patients. These results show that it is possible to detect numerical chromosomal changes and oncogene amplification in bone marrow micrometastatic epithelial cells of cancer patients by combining immunophenotyping and FISH.
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PMID:Detection of genetic alterations in micrometastatic cells in bone marrow of cancer patients by fluorescence in situ hybridization. 863 Sep 85

The structure and expression pattern of a human gene located within a homozygously deleted region of a metastatic prostate cancer have been characterized. Multiple cDNA fragments of this gene were isolated by hybrid capture with yeast artificial chromosome clones covering the deletion region. Eleven coding exons spanned 205-220 kb of the 730- to 970-kb deletion. The predicted amino acid sequence was 43% identical to that of an anonymous Caenorhabditis elegans gene and 20% identical to an accessory or regulatory subunit of the oligosaccharyltransferase enzyme complex in Saccharomyces cerevisiae. Hydrophobicity profiles of all three gene products were similar and showed four putative membrane-spanning domains in the molecules' C-terminal halves, suggesting a general conservation of function. The gene was expressed as an approximately 1.5-kb mRNA in most nonlymphoid human cells/tissues including prostate, lung, liver, and colon. Expression was detected in many epithelial tumor cell lines, but was undetectable by Northern blot or RT-PCR in 14 of 15 colorectal, 1 of 8 lung, and 1 of 4 liver cancer cell lines. Lack of expression in tumor cell lines was highly correlated with hypermethylation of a CpG island located at the gene's 5' end. These findings form a basis for further work on this candidate tumor suppressor gene.
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PMID:Structure and methylation-associated silencing of a gene within a homozygously deleted region of human chromosome band 8p22. 866 Nov 4

Normal rat prostate epithelial cells (EPYP-1) were isolated and immortalized with the Simian Virus-40 (SV40) large T-antigen, and transfected with the v-H-ras (EPYP-1-ras) and the c-myc oncogenes (EPYP-1-myc; EPYP-1-ras-myc) to serially create a step-wise model of tumor development in the rat prostate. Pronounced morphological differences were observed between EPYP-1 and the transfected sublines. The immortal epithelial cells (EPYP-1) maintained a cuboidal shape with orderly, contact mediated inhibition of growth. Oncogene transfected clones displayed a spindle shaped structure with multiple overlapping pseudopodia. Transfected cells also exhibited a greater degree of dysplasia, loss of contact inhibition growth and the upregulation of an epithelial tumor marker, cytokeratin-18. All cells exhibited anchorage independent and androgen independent growth. In vivo, EPYP-1 cells and EPYP-1-myc and formed slowly growing non-metastatic, benign tumors in immune compromised mice, while EPYP-1-ras and EPYP-1-ras-myc transfected cells produced rapidly growing, malignant tumors in similar animals. This model augments the hypothesis that tumor initiation and progression can be caused by as few as two discrete genetic events. In addition, the "normal" rat prostate epithelium and transfected daughter cell lines represent a tumor model system with distinct, well understood genetic alterations: activation of ras and myc. This model will be a valuable addition to the current cell lines used in the investigation of prostate cancer carcinogenesis.
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PMID:A model to study c-myc and v-H-ras induced prostate cancer progression in the Copenhagen rat. 976 99

The role of the neurotrophins (NTs) and their corresponding receptors (NTRs) TrkA, TrkB, TrkC, and p75NTR in neoplasia has received relatively little attention. However, because malignant cell migration within the prostate occurs predominantly by direct extension around prostatic nerves, the presence and possible upregulation of NTs from autocrine/paracrine sources and NTR expression within prostate epithelial tumor cells may be important in metastasis. We have been addressing their expression and interactions in human prostate cancer cell lines (LNCaP, PC-3, and DU145) and their role in prostate cancer invasion. In this study, we demonstrated that nerve growth factor (NGF), the prototypic NT, and NT-4/5 increased in vitro invasion through a reconstituted basement membrane and induced time- and dose-dependent expression of heparanase, a heparan sulfate-specific endo-beta-D-glucuronidase, an important molecular determinant of tumor metastasis. The NT effects were most marked in the DU 145 brain-metastatic cells and were detected at NT concentrations sufficient to fully saturate both low- and high-affinity NTRs. Additionally, we characterized the molecular expression of NT high-affinity (Trk) and low-affinity (p75NTR) receptors in these cell lines by reverse transcription-polymerase chain reaction. These lines had negligible trkA and trkC expression, although trkB was expressed in the three prostatic tumor cell lines examined. The brain-metastatic DU 145 cells were also positive for p75NTR. Our data showed that the NTs and NTRs are important in metastasis and that their expression coincides with transformation to a malignant phenotype capable of invasion along the perineural space and extracapsular metastasis to distant sites. These findings set the stage for more research into this area as related to prostate cancer evolution and may improve therapy for prostate cancer metastasis.
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PMID:Role of neurotrophins and neurotrophins receptors in the in vitro invasion and heparanase production of human prostate cancer cells. 1054 17

Bone marrow is a major homing site for circulating epithelial tumor cells. The present study was aimed to assess the proliferative capacity of occult metastatic cells in bone marrow of patients with operable solid tumors especially with regard to their clinical outcome. We obtained bone marrow aspirates from 153 patients with carcinomas of the prostate (n = 46), breast (n = 45), colon (n = 33), and kidney (n = 29). Most of the patients (87%) had primary disease with no clinical signs of overt metastases [tumor-node-metastasis (TNM)-stage UICC (Union Internationale Contre le Cancer) I-III]. After bone marrow was cultured for 21-102 days under special cell culture conditions, viable epithelial cells were detected by cytokeratin staining in 124 patients (81%). The cultured epithelial cells harbored Ki-ras2 mutations and numerical chromosomal aberrations. The highest median number of expanded tumor cells was observed in prostate cancer (2,619 per flask). There was a significant positive correlation between the number of expanded tumor cells and the UICC-stage of the patients (P = 0.03) or the presence of overt metastases (P = 0.04). Moreover, a strong expansion of tumor cells was correlated to an increased rate of cancer-related deaths (P = 0.007) and a reduced survival of the patients (P = 0.006). In conclusion, the majority of cancer patients have viable tumor cells in their bone marrow at primary tumor diagnosis, and the proliferative potential of these cells determines the clinical outcome.
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PMID:Heterogeneous proliferative potential of occult metastatic cells in bone marrow of patients with solid epithelial tumors. 1185 19


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