Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027627 (metastases)
 103,950 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A thyroid tumor cell line has been established from the metastases of a follicular carcinoma in a female patient. Although the primary tumor released thyroglobulin (Tg) into the circulation (greater than 10,000 ng/ml), the uptake of I131 was less than 2%. After 37 replications the doubling time was 4 days and confluency was reached after 7 days from inoculation of 3 x 10(7) cells. This human thyroid tumor cell line has now been growing in culture for several years. An aneuploid chromosomal pattern was observed (62-82 chromosomes). A pair of X chromosomes was present but no Y chromosome was found which is compatible with the female origin of the cell line. EM studies revealed the presence of microvilli. Immunoperoxidase staining using specific anti-human Tg antisera indicated the presence of Tg within the cells. Nude mice developed solid-cystic tumors within 6 months after injection of the cells. The basal release of immunodetectable Tg, as measured in a perifusion system, increased in response to thyroid stimulating hormone (TSH) (P less than 0.025) or TSH combined with theophylline (P less than 0.001). Unusual isoenzyme patterns for galactose-1-phosphate-uridyltransferase (GALT) and phosphoglucomutase1 (PGM1) were detected in the tumor, compared with normal human fibroblasts and blood cells and isoenzyme patterns from the patient's lymphocytes. Because this malignant human thyroid follicular cell line has retained the ability to synthesize Tg it represents a valuable model for the study of human follicular carcinomas.
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PMID:Characterization of a human follicular thyroid carcinoma cell line (UCLA RO 82 W-1). 257 Apr 83

Ricin A chain immunotoxin (IT) 45-2D9-RTA mediates regression of spontaneous pulmonary metastases and lung colonies from K-ras transformed rat fibroblasts (TRF cells). However, residual metastases are frequently noted after IT therapy, and therefore, possible mechanisms mediating tumor cell escape were investigated. Individual lung colonies were dissected from lungs of BALB/c mice, and single-cell suspensions of fresh cells from short-term cultures (eight passages) were tested. Immunoperoxidase staining with 45-2D9 monoclonal antibody showed that stable loss of surface antigen by cells cultured from IT-treated mice did not occur after four injections of specific IT. Sensitivity to specific IT in vitro was equal for metastatic tumor cells from mice treated with either two or four doses of specific IT compared to cells from nonspecific IT-treated mice and to parental cells. Clones derived from metastases of IT-treated mice were not resistant to IT. Clones derived from metastases of specific IT-treated mice internalized bound antibody or IT at the same rate as untreated cells. Freshly disaggregated cells from specific IT-treated mice were as sensitive to specific IT as were cells from nonspecific IT-treated or untreated mice. Specific IT successfully mediated reduction of lung colonies derived from fresh suspensions of lung colony TRF cells from IT-treated mice. This reduction was equivalent to that seen for cells not previously exposed to specific IT. Immunoperoxidase stains of lung sections with 45-2D9 showed that colonies consisting entirely of unstained TRF cells were present in both specific IT and phosphate buffered saline-treated mice. There was a trend toward a higher percentage of antigen-negative colonies in mice treated with IT, although 9 days following specific IT therapy, greater than 80% of lung colonies expressed gp74 antigen. When TRF cells were grown on agar plugs, which promoted three-dimensional growth, groups of cells showing absence of immunoperoxidase staining with antibody to gp74 were identified during 2 weeks of growth. Thus, stability of antigen-negative variants is favored by three-dimensional growth conditions and the selective pressure of IT administration. Our results also suggest that impaired trafficking of IT to antigen-positive cells may also contribute to escape from IT therapy.
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PMID:Analysis of gp74 expression by transformed rat fibroblasts from experimental pulmonary metastases following specific ricin A-chain immunotoxin therapy. 267 48

We set forth the results obtained after application of a hormonal protocol in prostate carcinoma (P.C.) on 257 patients controlled between June 1976 and June 1987, of whom we have selected 160 who fulfilled the following requirements: under 80 years old, confirmed anatomopathological diagnosis, state equal to or above the T1 of the Union International contre le Cancer (U.I.C.C.) classification, tolerance of treatment applied, clinical, analytical and complete, systematic iconographic follow up and minimum survival of more than one year. We treated those patients with localised P.C. (they have no demonstrable metastases), who in our series numbered 78 (78/160), with Diethylethylbestrol (D.E.S.) at an orally administered dose of 1 mgr. a day. In these the plasma testosterone dropped below 100 nanograms/l. in 57 cases (57/79). In this case metastases appeared in 22 cases (22/78). We treated those patients with metastatized P.C., who in our series numbered 59 (59/160), with orally administered Estramustine Phosphate (Estracyt) at a dose of 560 mgr. every 24 h. in two goes. In these the plasma testosterone dropped below 100 nanograms/l. in 50 cases (50/59). In this group the metastases disappeared in 7 patients, became stabilized in 30 and worsened in the other 22 patients. We carried out surgical orchiectomy on 49 patients (49/160): in 17 cases due to associate vascular pathology, in 13 cases for sociocultural reasons, in 5 cases because of advanced age and in 14 cases it was conducted on patients with a poor response to D.E.S.
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PMID:[Hormonal treatment of cancer of the prostate]. 267 37

A correlation between increased beta-1,6 branching of N-linked carbohydrates and the ability of a cell to metastasize or to form a tumor has been observed in several experimental models. Lec9 Chinese hamster ovary (CHO) mutants exhibit a drastic reduction in tumorigenicity in nude mice, and this phenotype directly correlates with their ability to attach an increased proportion of beta-1,6-branched carbohydrates to the G glycoprotein of vesicular stomatitis virus (J. Ripka, S. Shin, and P. Stanley, Mol. Cell. Biol. 6:1268-1275, 1986). In this paper we provide evidence that cellular carbohydrates from Lec9 cells also contain an increased proportion of beta-1,6-branched carbohydrates, although they do not possess significantly increased activity of the beta-1,6 branching enzyme (GlcNAc-transferase V). Biosynthetic labeling experiments show that a substantial degree of underglycosylation occurs in Lec9 cells and that this affects several classes of glycoproteins. Lec9 cells synthesize ca. 40-fold less Glc3Man9GlcNAc2-P-P-lipid and ca. 2-fold less Man5GlcNAc2-P-P-lipid than parental cells do. In addition, Lec9 cells possess ca. fivefold less protein-bound oligosaccharide intermediates, and one major species is resistant to release by endo-beta-N-acetylglucosaminidase H (endo H). Membranes of Lec9 cells exhibit normal mannosylphosphoryldolichol synthase, glucosylphosphoryldolichol synthase, and N-acetylglucosaminylphosphate transferase activities in the presence of exogenous dolichyl phosphate. However, in the absence of exogenous dolichyl phosphate, mannosylphosphoryldolichol synthase and glucosylphosphoryldolichol synthase activities are reduced in membranes of Lec9 cells, indicating that membranes of Lec9 cells are deficient in lipid phosphate. This was confirmed by analysis of lipids labeled by [3H]mevalonate, which showed that Lec9 cells have less lipid phosphate than parental CHO cells. Mechanisms by which a defect in the synthesis of dolichol-oligosaccharides might alter the degree of beta-1,6 branching in N-linked carbohydrates are discussed.
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PMID:Control of carbohydrate processing: increased beta-1,6 branching in N-linked carbohydrates of Lec9 CHO mutants appears to arise from a defect in oligosaccharide-dolichol biosynthesis. 272 6

Magnetic resonance (MR) imaging was performed on 14 patients with histologically proved osteosarcoma (mean age, 14.4 years). There was excellent correlation of intramedullary tumor extent as determined with MR imaging and pathologic examination (r = 99%). This was facilitated by the presence of a chemical shift artifact at the tumor-marrow interface on the T1-weighted images. The correlation between CT and pathologic findings was not as good (r = 84%). In a single patient, however, a 10-cm length of sclerotic bone was incorrectly interpreted as being tumor. If this case is excluded, the correlation between CT and pathologic findings improves significantly (r = 96%). T2-weighted images were optimal in demonstrating soft-tissue bulk and breach of the epiphysis or cortex. Vascular involvement was also readily defined. The T2 value of the tumor soft-tissue component decreased in patients who were deemed to have responded well to therapy. Two patients with very high T2 values after chemotherapy developed wide-spread metastatic disease and died. Phosphorus-31 MR spectroscopy of five patients with osteosarcoma showed elevated levels of phosphomonoesters (PMEs), inorganic phosphate (Pi), and phosphodiesters (PDEs). PME and PDE peak areas decreased in three patients after chemotherapy, while Pi peak areas increased.
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PMID:Osteosarcoma: use of MR imaging and MR spectroscopy in clinical decision making. 277 93

Using 31P-MR spectroscopy spectra with good signal-to-noise ratio were obtained in five different types of tumours (Ewing's sarcoma, osteosarcoma, malignant melanoma, metastases from a squamous cell carcinoma, parotid adenoma). Surface coils were used. Short- and long-term follow-up after chemotherapy was possible in some cases. In the short-term follow-up, changes in the phosphocreatine and inorganic phosphate resonances could be observed within minutes after the start of the infusion. In the longer follow-ups, changes in phosphodiester and phosphomonoester resonances were observed within two days. There were no significant changes in tissue pH during treatment, but increased pH values were observed in all tumours.
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PMID:[In vivo 31 phosphorus spectroscopy of tumors: pre-, intra- and post-therapy]. 284 3

Selective reticuloendothelial (RE) cell uptake of ethiodized oil emulsion 13 (EOE-13), an emulsion of Ethiodol (ethiodized oil) roentgenographic contrast material in a phosphate buffer, permits detection of small metastatic lesions of the liver and spleen through enhancement of roentgenographic density differences on computerized tomography (CT) between tissues containing and not containing RE cells. To determine the efficacy of this contrast material in the assessment of patients with metastatic disease of the liver, routine CT and emulsion enhanced tomography (EOE) were performed in a series of 15 patients prior to surgical exploration for treatment of carcinoma of the colon and rectum. All patients were suspected of harboring hepatic metastasis on the basis of clinical examination, liver function tests or radionuclide scans. EOE consistently demonstrated the nature and location of hepatic defects. Surgical exploration failed to locate one metastasis that was judged to be real because of progressive enlargement on EOE and CT over a period of two years. CT scans detected metastases in three patients subsequently shown to have normal livers and failed to detect disease in one patient subsequently shown to have metastases. EOE contrast material provides a more sensitive and accurate picture of metastatic liver involvement from carcinoma of the colon and rectum than is available on routine CT. The information provided by the results of this test can be useful in preoperative planning when treatment of disease of the liver is considerable feasible.
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PMID:Ethiodized oil emulsion enhanced computerized tomography in the preoperative assessment of metastases to the liver from the colon and rectum. 300 41

To investigate the role of oncogenes in the development of metastatic ability by prostatic cancer, the viral-Harvey-ras (v-H-ras) oncogene was introduced into the Dunning rat prostate adenocarcinoma cell line, AT2.1 by means of DNA transfection. The AT2.1 cell line is a cloned cell line that is anaplastic, rapidly growing, and has low metastatic potential; after subcutaneous (s.c.) inoculation in syngeneic rats, fewer than 10% of inoculated rats develop distant metastases. Calcium phosphate mediated DNA transfections of AT2.1 cells were performed with the v-H-ras oncogene or with control DNA. The in vitro growth rate of cloned transfectants, which contain and express the v-H-ras oncogene is similar to that of untransfected AT2.1 cells and of control transfectants. After s.c. inoculation in syngeneic rats, all transfectants produced rapidly growing tumors with similar growth rates. While control transfectants had low metastatic ability comparable to untransfected AT2.1 cells, the H-ras expressing transfectants metastasized in over 80% of inoculated rats. While the mechanism by which nonmetastatic Dunning tumor sublines spontaneously develop high metastatic ability in vivo during serial s.c. passage has not been addressed in the present studies, these studies do demonstrate that expression of an activated H-ras oncogene can reproducibly convert a tumorigenic nonmetastatic prostatic cell line to a highly metastatic state.
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PMID:Expression of a transfected v-Harvey-ras oncogene in a Dunning rat prostate adenocarcinoma and the development of high metastatic ability. 305 38

The mechanism by which the murine fibrosarcoma clone PAK 17.15 induces platelet aggregation [tumor cell-induced platelet aggregation (TCIPA)] was studied because platelet activation by this clone is necessary for metastasis to the lungs. PAK 17.15 TCIPA was completely inhibited by ADP-clearing enzymes, such as apyrase, or a mixture of creatine phosphate and creatine phosphokinase. Thrombin and collagen were not involved in PAK 17.15 TCIPA. Further studies showed that ADP is most likely secreted from activated platelets and that membrane protein(s) on PAK 17.15 cells are responsible for platelet activation. Inasmuch as ADP-dependent platelet aggregation requires fibrinogen and can be inhibited by the Gly-Arg-Gly-Asp-Ser (GRGDS) synthetic peptide, the effect of this peptide on PAK 17.15 TCIPA was studied. PAK 17.15 TCIPA was completely inhibited by the GRGDS peptide (0.4 mM) but not by a control peptide, Gly-Arg-Gly-Glu-Ser (0.8 mM). In addition, the GRGDS peptide inhibited adhesion of PAK 17.15 cells to immobilized fibronectin. As expected, the GRGDS peptide almost completely inhibited lung colonization by iv injected PAK 17.15 cells in C57BL/6 mice. Our results indicate that GRGDS may inhibit pulmonary metastases by interfering with TCIPA as well as with tumor cell adhesion to extra-cellular matrix components in the host.
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PMID:Inhibition of tumor cell-induced platelet aggregation and experimental tumor metastasis by the synthetic Gly-Arg-Gly-Asp-Ser peptide. 318 95

Immunological analysis is complementary of morphological analyses in the detection of neuroblastoma BM metastases. It attests the neuroblastic nature of rare pseudolymphocytic isolated cells. The combination of immunocytochemical technique (alkaline phosphate) and double-immunofluorescence technique allows the detection of as few as 10(-5) residual neuroblastoma cells. At the time of bone marrow harvest, it permits a precise evaluation of malignant cells in the graft.
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PMID:[Value of immunological analysis for the detection of residual neuroblasts in the bone marrow]. 328 77


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