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

Intraperitoneal gelatin sponge can mimic a mass lesion on magnetic resonance (MR) images. To determine the MR imaging characteristics of gelatin sponge over time, a 15 x 10 x 4-mm piece of gelatin sponge soaked in saline was surgically implanted in the peritoneal cavity of 14 mice. Two mice underwent a sham operation. Contiguous axial spin-echo images of the abdomen were obtained with T1-weighted, spin-density, and T2-weighted sequences preoperatively and over a 6-week period postoperatively. Gelatin sponge initially appears as a heterogeneous mass of low signal intensity on T1-weighted images and increasing intensity on spin-density and T2-weighted images, containing multiple round foci of very low signal intensity, attributable to air, at all sequences. Over time, signal intensity further increases and becomes more homogeneous on spin-density and T2-weighted images, although foci of air persist to 3 weeks. By 2-4 weeks, the mass is no longer discrete. Foci of air should help differentiate gelatin sponge from tumor and add gelatin sponge to the differential diagnosis of abscess.
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PMID:MR imaging appearance of intraperitoneal gelatin sponge in mice. 162 82

Tumor proteinases are considered to be important in the process of cancer invasion and metastasis. We have proposed that the surface membrane localization of these proteinases places them in an optimal site to facilitate the invasion of surrounding extracellular matrix. In this study, we have used the organic solvent, n-butanol, and the detergent, n-octyl-glucoside, to sequentially extract metalloproteinases from crude plasma membranes of human RWP-I pancreatic cancer cells. Anion exchange chromatography and gel permeation chromatography were employed to further purify enzymes with the capacity to degrade gelatin, type-IV collagen, and carboxymethylated transferrin. Gelatin zymography was used to demonstrate proteinase bands of 92, 70 and 62-kDa. Immunoblotting of solubilized, partially purified pancreatic cancer plasma membrane proteins using polyclonal rabbit antibodies, which have specificity for type-IV collagenase/gelatinase, resulted in the recognition of a 70-kDa protein, but not the 92-kDa gelatinase. A type-IV collagenase/gelatinase of 68-kDa was similarly identified in A2058 human melanoma cancer cell plasma membranes.
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PMID:Extraction of type-IV collagenase/gelatinase from plasma membranes of human cancer cells. 216 1

The role of epidermal growth factor in the regulation of the proteolytic and RBC cytolytic activity of the A431 cancer cell line has been evaluated using our previously described gelatin/polyacrylamide electrophoretic assay and tumor-induced RBC cytolysis assay, respectively. A431 cells maintained in 10% fetal bovine serum were actively cytolytic for RBC (release index, 53.0 +/- 2.9%), whereas serum-starved cells maintained in serum-free medium were not cytolytic for RBC. RBC cytotoxicity was restored by adding as little as 3.4 pM epidermal growth factor to the serum-deprived cells. The RBC cytolytic stimulating activity of epidermal growth factor could be mimicked by the metal chelating agent 1,10-phenanthroline, suggesting a possible role for calcium ions in the action of epidermal growth factor and proteases. An enriched cell membrane preparation of A431 cells was also cytolytic for RBC but was unaffected by metal chelating agents. RBC-induced cytotoxicity was inhibited by the protease inhibitor leupeptin. Gelatin substrate gels of enriched A431 cell membrane preparations and serum-free supernatants revealed a pattern of high- and low-molecular-weight proteases that were stimulated by metal chelators and inhibited by leupeptin. The activity of these proteases appears to be regulated by epidermal growth factor by a process that may involve divalent cations.
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PMID:Role of epidermal growth factor in the expression of A431 cancer cell protease and red blood cell cytotoxicity. 249 51

A case of bilateral renal angiomyolipoma without tuberous sclerosis is reported. A 49-year-old woman was admitted to the general practitioner with a sudden onset of severe left flank pain. An excretory urogram and ultrasonogram revealed an enlargement of the left kidney. She was subsequently referred to our clinic for further investigation and treatment. Computed tomographic scan and magnetic resonance imaging using Tl-weighted image showed several tumors with a fatty, dense area in the bilateral kidney. An arteriogram demonstrated a hypervascular renal mass with aneurysms in her left kidney. Diagnosis of bilateral renal angiomyolipoma was confirmed by percutaneous needle biopsy. Superselective embolization of the tumor was successfully performed, preserving normal renal tissue. Gelatin sponges containing Carboquone (CQ sponge) were used as embolic material. Angiomyolipoma has become relatively easy to diagnose by CT, ultrasound, MRI and so on. However, there are some cases of angiomyolipoma which are indistinguishable from renal cell carcinoma using these modes of testing. Therefore, in selecting a conservative management, we indicated that percutaneous biopsy or open biopsy should be done to confirm the results of the above procedures. Moreover, therapeutic embolization for angiomyolipoma was concluded to be very useful.
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PMID:[Therapeutic embolization of renal angiomyolipoma: a case report]. 280 11

Connective tissue matrix-degrading metalloproteinases play an important role in cancer invasion. In this report we describe the isolation of a metalloproteinase exhibiting both type IV collagenolytic and gelatinolytic activities from the conditioned medium of NIH-3T3 fibroblasts transformed with DNA containing an activated c-Harvey-ras oncogene from T24 bladder cancer cells. This tumor proteinase was purified by anion exchange chromatography, zinc-chelate Sepharose chromatography, and gel permeation chromatography. The final product was homogeneous on sodium dodecyl sulfate-polyacrylamide gel electrophoresis (relative molecular mass = 67,000). Gelatin zymography revealed two bands of gelatinolytic activity, corresponding to molecular weights of 67,000 and 62,000. Upon immunoblotting with the use of an affinity-purified polyclonal rabbit antibody to a peptide region of type IV collagenase that lacks homology with interstitial collagenase or stromelysin, the purified tumor enzyme was identified as type IV collagenase.
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PMID:Purification of a gelatin-degrading type IV collagenase secreted by ras oncogene-transformed fibroblasts. 284 10

Gelatin microspheres containing recombinant human interferon alpha A/D (A/D-IFN) (IFN-microspheres) potentiated the antitumor activity of mouse peritoneal macrophages (M phi) much more efficiently than free A/D-IFN. M phi acquired the inhibitory activity on tumor cell growth by the ingestion of IFN-microspheres without the aid of lipopolysaccharide (LPS), though LPS was required as a second signal for activating M phi primed with free IFN. The IFN-microspheres were much more efficient than free IFN plus LPS in respect of the IFN amount and the time required for M phi activation. Furthermore, M phi pretreated with the IFN-microspheres maintained their activated state for a much longer period than those pretreated with free A/D-IFN plus LPS. A monoclonal anti-IFN-alpha A antibody, which was capable of neutralizing A/D-IFN, did not interfere with the M phi activation by the IFN-microspheres. Even human IFN-alpha A was effective in activating murine M phi similarly to A/D-IFN, when given in the form of IFN-microspheres, though human IFN-alpha A in the free form was ineffective. These results argue that the mechanism of M phi activation by the IFN-microspheres is different from that by free IFN.
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PMID:Potentiation of antitumor activity of macrophages by recombinant interferon alpha A/D contained in gelatin microspheres. 313 17

We have developed a new in vitro model system to examine tumor cell-platelet-endothelial cell interactions under dynamic conditions. Using the same model, we can determine endogenous eicosanoid metabolism and alterations in the prostacyclin-thromboxane A2 balance associated with interactions among tumor cells, platelets, and endothelial cells. The model consisted of cloned rat aortic endothelial cells grown on gelatin microcarrier beads under dynamic conditions (i.e., spinner culture). Interactions of these endothelial cells with platelets (heparinized rat platelet rich plasma) and/or tumor cells (rat Walker 256 carcinosarcoma) were assessed in an aggregometer. Gelatin beads alone or microcarrier grown endothelial cells did not elicit spontaneous aggregation of platelet rich plasma over a time period of 30 min. Microcarrier grown endothelial cells inhibited tumor cell induced platelet aggregation in a dose dependent fashion (i.e., depending on endothelial cell number). The ability of microcarrier grown endothelial cells to inhibit tumor cell induced platelet aggregation depended on endogenous production of prostacyclin. This conclusion is based on the following results: an increased number of microcarrier grown endothelial cells caused a prolongation of the aggregation lag time; an increased number of microcarrier grown endothelial cells caused a proportionate increase in 6-keto-prostaglandin F1 alpha concentration; an increased number of microcarrier grown endothelial cells was inversely correlated with thromboxane A2 production by platelets; indomethacin pretreatment of microcarrier grown endothelial cells caused a decrease in prostacyclin production and therefore overcame the associated inhibition of tumor cell induced platelet aggregation; and the inhibition of tumor cell induced platelet aggregation in the presence of endogenous prostacyclin produced by microcarrier grown endothelial cells was the same as that observed in the presence of exogenous prostacyclin. Scanning electron microscopy of aggregometry samples revealed: little or no platelet or tumor cell adhesion to gelatin beads alone, a low basal adhesion of tumor cells to microcarrier grown endothelial cells, and large aggregates of platelets and tumor cells located primarily at gaps in the monolayer of indomethacin treated microcarrier grown endothelial cells. This new in vitro model provides a method for examining the effects of eicosanoid metabolism by endothelial cells on tumor cell-platelet-endothelial cell interactions under dynamic conditions.
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PMID:A new in vitro model for investigation of tumor cell-platelet-endothelial cell interactions and concomitant eicosanoid biosynthesis. 355 14

We devised a model system to study the effects of extracellular matrix proteins on the malignant phenotype of an anaplastic glioma cell line, U 343 MG-A. Well-characterized cultures derived from normal human leptomeninges were grown to confluence and maintained for 2 weeks. The leptomeningeal cells were then removed with base and detergent, leaving behind an extracellular matrix enriched in laminin, fibronectin, type I and IV collagen, and procollagen III. U 343 MG-A tumor cells planted on top of this normal extracellular matrix were profoundly growth inhibited compared with glioma cells grown on plastic alone. Glioma cells grown on the extracellular matrix developed multiple, slender processes and assumed a more differentiated astrocytic phenotype; immunostains for glial fibrillary acidic protein revealed a more extensive intracytoplasmic network of intensely staining filaments than in control glioma cells. When glioma cells grown on the extracellular matrix were analyzed by an enzyme-linked immunosorbent assay for glial fibrillary acidic protein, the amount of this intermediate filament per cell was increased 20-fold compared with glioma cells growing on plastic. The growth and differentiation of U 343 MG-A glioma cells in flasks coated with purified fibronectin or laminin was not significantly perturbed; however, glioma cell cultures grown in flasks coated with purified type I or IV collagen showed decreased cellular proliferation, stellate cell formation, and increased levels of glial fibrillary acidic protein per cell compared with glioma cells growing on plastic. Gelatin gel analysis showed that U 343 MG-A glioma cells growing on plastic secreted a 65,000-D metalloproteinase that was not secreted by glioma cells grown on the leptomeningeal extracellular matrix. We conclude that in this system, the extracellular matrix of a normal human leptomeningeal culture substantially inhibited the proliferation of and induced differentiation in an anaplastic glioma cell line. Our analysis of single components of the extracellular matrix suggests that these effects may be mediated in part by type I and IV collagen. The mechanism by which the leptomeningeal extracellular matrix inhibits glioma cell proliferation may be by diminishing tumor-associated protease secretion so that the degradation of extracellular matrix macromolecules in the tumor cell microenvironment is prevented and tumor cell migration becomes less likely.
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PMID:Inhibition of growth and induction of differentiation in a malignant human glioma cell line by normal leptomeningeal extracellular matrix proteins. 355 73

A gelatin sponge model system for tumor cell inoculation and retrieval of tumor-associated leukocytes is described. Gelatin sponges pre-implanted in nude mice harboring tumorigenic Chinese hamster ovary cells (line CHO) were examined at 2 and 11 days after injection of tumor cells for tumor cell content and leukocyte accumulation after digesting the sponge matrix in collagenase solution. The data indicate a progressive influx of host cells consisting primarily of macrophages, neutrophils and lymphocytes. The total number of viable tumor cells as well as the fraction of surviving tumor cells with clonogenic potential also increased with tumor age. Blank sponges not harboring tumor cells elicited an inflammatory response in the animals which did not change appreciably with length of sponge residence. However, when the sponges were harboring tumor cells, the accumulation of host leukocytes far exceeded that which occurred in blank sponges. This observation suggests a host response directed toward the tumor which is absent in animals bearing blank sponges. Apart from providing anchorage for injected cells, the gelatin sponge, by virtue of its digestibility in collagenase, makes possible the easy retrieval and precise quantitation of tumor-associated host cells.
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PMID:A gelatin sponge model for studying tumor growth: quantitation of tumor cells and leukocytes in the CHO tumor. 359 90

We have found that a murine hepatoma displays a considerable phenotypic diversification in culture, which depends upon the substratum utilized, and is manifested by the formation of multicellular structures of differing geometry: Monolayer on glass and plastic, thick multilayer pads on Gelfilm, and spheroids on agar and agarose. These multicellular morphological phenotypes were assayed without disruption to ascertain their antigenicity in vitro and their tumorigenicity in vivo and to obtain quantitative information on the effect of the spatial arrangement of the hepatoma cells upon the ability of each multicellular structure to interact, as a whole, with molecules and cells in its surroundings. The antigenicity of the multicellular structures was determined with calibrated probes and a methodology that measures the total antigenicity, as well as antigenicity per unit of surface area. Antigenicity was found to differ in the following decreasing order: Monolayer on plastic greater than spheroids on agarose greater than spheroids on agar greater than multilayer on Gelfilm. At least part of these antigenic variants arise from different degrees of masking of the structures' surface determinants by a trypsin-sensitive material. The multicellular phenotypes also differed in tumorigenicity. When assayed in syngeneic hosts under comparable conditions, agar-grown spheroids produced the fewest tumors, whereas Gelfilm-grown multilayers produced the most. These two independent sets of data show that the various geometries that a tumor tissue is induced to acquire by the culture substratum are accompanied by a distinctive combination of surface and biological properties.
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PMID:Phenotypic diversification of a cultured tumor line as a function of substratum. 702 95


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