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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have developed and partially characterized a mouse model system for studying human prostate tumor cell metastases in vivo. To develop this model we have selected highly invasive (3 x I.) and non-invasive (3 x N.I.) PC-3 human prostatic tumor sublines based on enhanced and diminished capacities to migrate across a reconstituted basement membrane barrier (Matrigel) in Boyden chamber chemotactic assays. When the 3 x I. cells were injected intravenously (i.v.) in the tail vein of severe combined immune deficient (scid) mice, the cells initially metastasized to a wide variety of tissues as demonstrated by using [125I] IUdR labeled cells and histology. Four distinct sublines were eventually isolated which preferentially metastasized at approximately 80% efficiency to the lumbar vertebrae (PC-3 ML), the mandibular region of the right cheek (PC-3 MC), the rib cartilage (PC-3 MR), and the right front knee bone (PC-3 MK), respectively. Implantation experiments at different sites indicated that organ metastases may somehow be conferred on the tumor subclones by the host tissue.
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PMID:Isolation and characterization of PC-3 human prostatic tumor sublines which preferentially metastasize to select organs in S.C.I.D. mice. 177 17

TR3 receptor is a human homolog of mouse Nurr77 and N10 protein and the rat NGFI-B protein. A cDNA encoding a chimeric nuclear receptor composed of the N-terminal domain and C-terminal putative ligand-binding domain of the orphan receptor TR3 receptor and the DNA-binding domain of the androgen receptor was constructed. The chimeric receptor, called TR3/AR/TR3 receptor, when expressed in COS-1 monkey kidney cells or PC-3 human prostate tumor cells, cotransfected with an ARE-containing mouse mammary tumor virus long terminal repeat-linked reporter gene encoding chloramphenicol acetyltransferase (CAT), activated CAT expression in the absence of any added factor. The activation was dependent on the amount of expression vector transfected and appeared to be independent of the concentration of serum supplement. Intact TR3 receptor was not active in this system. A TR3/AR/TR3 receptor protein truncated in the putative ligand-binding domain also induced CAT activity. TR3 receptor appears to be a transcriptional factor that activates transcription independently of ligand or binds an endogenous ligand present constitutively in cultured cells.
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PMID:Transcriptional activation by TR3 receptor, a member of the steroid receptor superfamily. 184 11

Plasminogen activators (PA), particularly the lower Mr urokinase (u-PA) type, have been associated with tumor cell invasion and metastasis. We have examined the expression of PA by two human prostate cancer cell lines (PC-3 and DU-145) using functional and immunologic techniques. The culture media and cell extracts of the more aggressive PC-3 cell line contained more than two-fold greater PA activity than the relatively indolent DU-145 cell line. Zymographic studies identified the PA expressed as u-PA. PC-3 cells expressed an additional lower molecular weight form of u-PA not noted in DU-145 cells. Heterogeneity in u-PA expression was shown by the fibrin lysis assay, immunohistochemistry, and dual parameter flow cytometry indicating the presence of phenotypically divergent cell populations. Increased u-PA expression may identify those tumor cells that possess aggressive biological potential.
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PMID:Heterogeneity in plasminogen activator (PA) levels in human prostate cancer cell lines: increased PA activity correlates with biologically aggressive behavior. 190 92

We have established an animal model of bone metastasis using the PC-3 human prostate tumor cell line. In order to assess whether inhibition of bone resorption would prevent the development of bone metastasis, the diphosphonate etidronate (EHDP) was administered to 20 mice at a dose of 30 mg/kg subcutaneously daily starting 2 days prior to injection of tumor cells. Control mice received daily injections of the saline vehicle. In the EHDP-treated mice, there was no significant reduction in the incidence of bone metastasis, the size of the lesions, or the number of bone lesions per mouse. Approximately 50% of the mice developed bone metastasis, which was similar to the control group and similar to what was observed in earlier studies with this animal model. Histomorphometric analysis of bones showed marked inhibition of mineralization in EHDP-treated mice, thus indicating biological effect on the bone. Therefore, the use of EHDP in biologically effective doses failed to reduce the incidence, size, or number of bone metastases in this animal model.
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PMID:Effect of etidronate disodium on the development of bone lesions in an animal model of bone metastasis using the human prostate cancer cell line PC-3. 192 62

The effect of radiation and/or hyperthermia on a human prostatic carcinoma xenograft in athymic nude mice was investigated. A human prostate carcinoma subline (1-LN-PC-3-1A) was inoculated subcutaneously in the thigh of male athymic nude mice. When tumors reached a size of approximately 200 mm.3, they were treated with either radiation (X) or hyperthermia (H) alone, or in combination (X + H). In the combined treatment, hyperthermia was delivered immediately after radiation exposure. Comparison of the time required to reach twice the tumor volume observed at the time of treatment was used to define therapeutic impact on tumor growth. The combined treatment resulted in median tumor volume doubling time of 35.5 days, compared to 18 days and 25.5 days, respectively, for hyperthermia or radiation alone. Analysis of tumor doubling time using a proportional hazards regression indicates that under the conditions of this experiment, the effect of radiation and hyperthermia for 1-LN-PC-3-1A tumors is additive. The impact of this treatment regimen in the management of prostatic cancer requires further investigation.
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PMID:The effect of radiation therapy and hyperthermia on a human prostatic carcinoma cell line grown in athymic nude mice. 199 25

Transformed fibroblasts coinoculated with epithelial cells accelerated the growth and shortened the latency period of human epithelial tumors in athymic mice. Addition of NbF-1 fibroblasts caused epithelial tumors to grow from five marginally tumorigenic or "nontumorigenic" (nontumor-forming) human tumor cell lines or strains: PC-3 (prostate), WH (bladder), MDA-436 (breast), and cells derived from the ascites fluids of patients with metastatic renal pelvic or prostate cancers. Evidence for the human and epithelial nature of these experimental tumors was provided by histologic, immunohistochemical, Southern and dot-blot hybridization, and cytogenetic analyses. Transformed fibroblasts induced predominantly carcinosarcomas, whereas nontumorigenic fibroblasts (NIH 3T3) and lethally irradiated transformed fibroblasts induced exclusively carcinomas. The fibroblast-epithelial interaction appears to occur bidirectionally and does not result from cell fusion. Because coculture experiments in vitro did not demonstrate an increased cell proliferation, it appears that undefined host factors can influence tumor growth. This tumor model may be useful in drug-screening programs and in mechanistic studies of factors regulating human tumor growth and progression.
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PMID:Fibroblast-mediated acceleration of human epithelial tumor growth in vivo. 229 6

We suspect a difference between the effective rate of human tumor clonogenic assay (HTCA) and that of clinical chemotherapy against renal cell carcinoma. We investigated the sensitivity of ACHN, the cell line of renal cell carcinoma, and its colony forming cells (dividing cells) obtained on double soft agar against vincristine sulphate (VCR). In addition, PC-3, a cell line of prostatic carcinoma, and HeLa, cell line of cervicar carcinoma, were investigated. We obtained the results that each colony forming cells had higher sensitivity than each parent cells against VCR in the growth activities and the DNA synthesis measured by the uptake of 3H-thymidine. Because the cells targeted by HTCA are dividing cells, they are oversensitive compared with the true sensitivity of tumors.
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PMID:[Study on chemosensitivity of colony forming cells]. 232 17

A study was made on 2 types of 131I-labeled anti-CA 19-9 and anti-CEA mouse monoclonal antibodies (IMACIS-1) against human cancer related antigen as to their usefulness in radioimmunoimaging. Tumor-bearing nude mice were used for comparison. The transplanted tumors (SW948, COLO 201) were clearly visualized 48-72 hours after administration of IMACIS-1. Tumor/blood ratio 72 hours after administration: 8.69 in COLO 201 and 5.70 in SW948, showing ca. 10-15 times as high as those in PC-3 and HEp-2. IMACIS-1 therefore is considered useful in radioimmunoimaging of cancer. Analysis was made by in vitro cell ELISA. As a result, both of the cells specifically reacted with anti-CA 19-9 but not anti-CEA.
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PMID:[A fundamental study of immunoscintigraphy with 131I-labeled anti-CA 19-9 and anti-CEA monoclonal antibodies--imaging of tumor-bearing mice by IMACIS-1 and cell ELISA with human tumor cells]. 239 26

The human prostate tumor subline 1-LN-PC-3-1A (1-LN) is reproducibly metastatic in adult athymic nude mice. Cells surviving a brief in vitro exposure to ethyl methanesulfonate (EMS) exhibited a profound decrease in capacity for experimental lung metastasis in nude mice. Thirty days after EMS treatment, 1 X 10(6) uncloned EMS-treated 1-LN cells (1-LN-EMS-10) were injected IV into groups of 6 to 8-week-old male athymic nude mice (BALB/cAnBOM). A median of 8.5 colonies/lung was observed among 20 1-LN-EMS-10-injected mice, which was significantly different from the median of 51 colonies/lung produced among 14 1-LN-injected mice (P = 0.0002). This altered phenotype remained stable during 150 days of continuous culture. However, the 1-LN-EMS-10 cells were tumorigenic in 10/10 nude mice injected SC. Single lung tumor colonies recovered from 1-LN-EMS-10-injected mice and reinjected IV into nude mice produced medians of 32-63 colonies/lung. The altered metastatic phenotype resulting from treatment of 1-LN with EMS was reversed by exposure to a noncytotoxic dose of 5-azacytidine, but unaffected by a second exposure to EMS. Collectively these data demonstrate that the metastatic phenotype of these human tumor cells in athymic nude mice can be heritably altered by in vitro exposure to EMS and 5-azacytidine. Analysis of the mechanisms underlying these phenotypic changes may provide insight into parts of the complex process of tumor cell evolution.
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PMID:Metastatic phenotype of human prostate tumor cells in athymic nude mice: alteration by exposure to ethyl methanesulfonate and "reversion" by 5-azacytidine. 241 1

Parallel in vitro exposure to 5-azacytidine or to ethyl methanesulfonate either significantly reduced or had no major impact on the experimental metastasis capacity of different clones of the human prostatic carcinoma subline 1-LN-PC-3-1A. The impact of these agents on metastatic capacity varied (1) among different clones and (2) between clones and the uncloned parental line. Analysis of the process by which these agents modify the metastatic phenotype of human tumor cells may offer insight into the process of phenotypic diversification.
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PMID:Clonal variation in the impact of ethyl methanesulfonate and 5-azacytidine on the metastatic phenotype of human prostatic tumor cells in athymic nude mice. 246 29


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