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At least 1,369 records · Page 76Linked to original sources
PubMed1997

Urokinase-type plasminogen activator receptors associate with beta1 and beta3 integrins of fibrosarcoma cells: dependence on extracellular matrix components.

We have shown previously that the urokinase-type plasminogen activator receptor (uPAR) physically associates with beta2 integrins on human leukocyte membranes. We now report that uPAR associates with certain members of the beta1 and beta3 integrin families expressed by a nonhematopoietic fibrosarcoma cell line (HT1080) when adherent to certain extracellular matrix molecules. Flow cytometry studies indicated that HT1080 cells expressed uPAR and beta1 and beta3 integrins. Double staining immunofluorescence was used to label uPAR and beta1 and beta3 integrins. The staining patterns of uPAR and beta1 integrins were strikingly similar when attached to fibronectin, laminin, or vitronectin but not polylysine-coated substrates. Resonance energy transfer (RET) between uPAR and beta1 integrins was observed, especially at focal adhesion plaques; this indicates that these molecules are within about 7 nm of each other on these cell membranes. uPAR and beta3 integrin coclustering and RET were also observed on tumor cells adherent to vitronectin but not to fibronectin, laminin, or polylysine-coated surfaces. Because N-acetyl-D-glucosamine was found previously to inhibit beta2 integrin-uPAR association, we tested the effect of saccharides on the beta1-uPAR and beta3-uPAR colocalization and RET. Colocalization and RET between uPAR and beta1 or beta3 integrins were effectively inhibited by N-acetyl-D-glucosamine on extracellular matrix-coated surfaces. To better define which members of beta1 and beta3 integrin families associate with uPAR, we studied the association of several alpha subunits with uPAR on tumor cells. We found that: (a) alpha5 colocalizes with uPAR on cells attached to fibronectin-coated surfaces; (b) alpha5 and alpha(v) colocalize with uPAR on cells adherent to vitronectin; and (c) alpha3 and alpha6 associate with uPAR on cells attached to laminin. In further support of physical associations between integrins and uPAR on tumor cells, uPAR was found to coimmunoprecipitate with beta1 integrins in Brij-58 lysates of HT1080 cells (as detected by anti-uPAR Western blotting of material isolated from an anti-beta1 integrin immunoaffinity column). Thus, uPAR may laterally associate with integrins of tumor cells when attached to specific extracellular matrix elements to enable directional proteolysis for tumor cell migration and invasion.

Antibodies, Monoclonal↗
PubMed1997

Lameness and pleural effusion associated with an aggressive fibrosarcoma in a horse.

An 8-year-old Thoroughbred gelding was admitted for evaluation of chronic lameness of the left scapulohumeral joint of 3 months' duration. Radiography revealed a radiolucent lesion with the proximal portion of the humerus in the area of the metaphysis. Scintigraphy confirmed radiographic findings, with an increased uptake of technetium Tc 99m medronate in the proximal portion of the left humerus. A preliminary diagnosis of humeral fracture was made. Two weeks later, the horse was readmitted for clinical signs of respiratory distress. Radiographic and ultrasonographic evaluation revealed masses within the thoracic and abdominal cavities. The diagnosis was changed to neoplasm with multiple metastases. Because of the unfavorable prognosis, the horse was euthanatized. Necropsy findings confirmed an aggressive neoplasm. Special histochemical stains, immunohistochemistry, and electron microscopy were required to characterize the neoplasm as an anaplastic fibrosarcoma. Findings in this horse illustrate the importance of considering neoplasia, resulting in bone lesions, as a possible cause of chronic lameness in horses.

Animals↗
PubMed1997

Invasive properties of cadmium-resistant human fibrosarcoma HT-1080 cells.

Invasive properties of tumor cells having acquired heavy metal resistance were investigated. We selected the cadmium-resistant (Cd-R) cells from human fibrosarcoma HT-1080 cells. Total metallothionein levels in cytosol of HT-1080 Cd-R cells were significantly higher than original lines, and were of a highly resistant potency to cytotoxicity of cisplatin, as well as heavy metals. The HT-1080 Cd-R cells showed higher invasiveness into recombinant basement membrane Matrigel. However, HT-1080 Cd-R cells were inferior in locomotion ability. Significant differences in adhesive ability to extracellular matrix proteins were not observed between HT-1080 and HT-1080 Cd-R cells. High invasiveness of HT-1080 Cd-R cells was caused by their extremely strong enzymatic activities. High level of 92kDa matrix metalloproteinase-9 (MMP-9) was recognized from the conditioned medium of HT-1080 Cd-R cells, whereas 72kDa MMP-2 was secreted equally from both cell lines. Our investigation suggests that drug resistance acquired through the mechanisms of cellular metal-tolerance may promote malignancy and tumor metastasis during cancer chemotherapy.

Cadmium↗
PubMed1997

Carrier-mediated transport of oligopeptides in the human fibrosarcoma cell line HT1080.

To explore the feasibility of targeting human tumor cells via their transport systems, dipeptide uptake was studied in the human fibrosarcoma cell line HT1080 and the human fibroblast cell line IMR-90 by the use of hydrolysis-resistant glycylsarcosine (Gly-Sar). The uptake of [14C]Gly-Sar into HT1080 was time dependent. Kinetic analysis of the concentration dependence of the initial rate of [14C]Gly-Sar uptake showed that a carrier-mediated transport system with a K(m) of 11.4 +/- 3.3 mM and V(max) of 26.8 +/- 4.0 (nmol/15 min/mg protein) and a nonsaturable component (k(d) of 0.80 microl/15 min/mg protein) were responsible for the dipeptide uptake by HT1080 cells. The optimal pH for the maximal uptake was around 6.0. [14C]Gly-Sar uptake was inhibited by various di- and tripeptides and peptide-mimetic drugs, such as bestatin and cefadroxil. [14C]Gly-Sar uptake was not affected by the presence of amino acids or tetra- or pentapeptides. The uptake of cefadroxil was reduced significantly by unlabeled Gly-Sar. Moreover, Gly-Gly and Gly-Leu produced an increase in the apparent K(m) of the uptake of Gly-Sar without altering V(max). On the other hand, dipeptide uptake by IMR-90, which is a normal diploid cell line (not malignant), showed no saturable transport. These results suggest that HT1080 cells take up dipeptides via a pH-dependent transporter. This is the first report showing that a dipeptide transport system, which is similar but not identical to the well-characterized oligopeptide transporters PepT1 and PepT2, exists in fibroblast-derived tumor cells but not in normal fibroblasts. The present finding could be the basis of a novel strategy for the specific delivery of oligopeptide-mimetic anticancer drugs into tumor cells.

Biological Transport↗
PubMed1996

[Invasion of fibrosarcoma cells transfected with PAI-2 gene].

The effect of PAI-2 on the invasion of fibrosarcoma cells in vitro and in vivo was investigated. The control cells (C+, C+ pem) and PAI-2 transfectants (C+ exp) were used in the assay of the degradation of isotopically labelld 3H-ECM and were injected sc into athymic/nude mice. Recombinant PAI-2 could inhibit efficiently the degradation of 3H-ECM by tumor cells (86.5%). The PAI-2 transfectants remained tumorigenic in nude mice, but tumors originating from the PAI-2 transfectants showed histologically the presence of a thick capsule which was absent in tumors from control cells.

Animals↗
PubMed1997

Overexpression of manganese superoxide dismutase selectively modulates the activity of Jun-associated transcription factors in fibrosarcoma cells.

Manganese superoxide dismutase (MnSOD) is reduced in a variety of tumor cells and has been proposed to be a new type of tumor suppressor gene. The mechanism(s) by which MnSOD suppresses cancer development is currently unknown. However, expression of this antioxidant might play a significant role in maintaining cellular redox status. The relationship between MnSOD expression and modulation of DNA-binding activity and transcriptional activation of redox-sensitive oncoproteins and tumor suppressor proteins was studied in a murine fibrosarcoma cell line (FSa-II). Electrophoretic mobility shift assay and transcriptional activation studies revealed an inverse correlation between MnSOD expression and activity of c-jun-associated transcription factors, activator protein 1 and cyclic AMP-responsive element binding protein. Furthermore, expression of an activator protein 1 target gene, bcl-xL, was decreased in MnSOD-transfected cell lines. The results suggest that overexpression of MnSOD may exert its tumor suppressor activity, in part, by modulation of specific oncogenes.

Animals↗
PubMed1997

Protein bound polysaccharide PSK abrogates more efficiently experimental metastases derived from H-2 negative than from H-2 positive fibrosarcoma tumor clones.

We studied the effect of protein-bound polysaccharide PSK on metastatic colonization of BALB/c mice after intravenous injections of different syngeneic murine H-2 positive and H-2 negative tumor clones. The tumor lines used were different clones from chemically induced fibrosarcomas (GR9.B9, an H-2 negative clone from GR9 tumor, and B7.1.B4, an H-2 positive clone from B7.1 tumor). These clones were selected because of their different sensitivity to NK cytotoxicity, which was related to MHC class I expression. Pretreatment of mice with PSK inhibited metastatic colonization derived from B9 H-2 negative tumor cells. In contrast, lung colonization of PSK treated mice injected with B7.1.B4 H-2 positive tumor cells was higher, and differences in the number of colonies between untreated and PSK treated mice were small. In several experiments the effect of PSK was attenuated to a greater degree when high numbers of cells were injected. Abrogation of NK cells with anti-asialo GM1 serum significantly increased (in all tumors and at different cell doses) the number of metastatic colonies in comparison with untreated mice injected with tumors, regardless of the cell dose used. These results clearly suggest that NK cell activation in vivo by the protein bound polysaccharide PSK abrogates metastasis formation in mice. Abrogation was dependent on the H-2 phenotype even when pretreatment consisted of a single dose of PSK. This effect, related to the NK sensitivity of the tumor target, can be used to predict the effect of PSK in vivo.

Animals↗
PubMed1997

Activity of lysosomal and nonlysosomal proteases and contents of protein and its degradation products in the blood serum of rats with fibrosarcoma induced by methylcholanthrene.

Activity of lysosomal and nonlysosomal proteases and contents of protein and its degradation products in the blood serum of rats with methylcholantrene fibrosarcoma were evaluated. Activity of lysosomal proteases and prolidase and prolinase as well in the blood serum of rats with methylcholanthrene tumour did not differ from the activity of these enzymes in the blood serum of control rats. Only the activity of elastase and collagenase in the blood serum of rats with methylcholanthrene tumour especially with tumour of intermediate and big mass was increased. Content of total protein was decreased in the blood serum of rats with tumour of intermediate and big mass and contents of glycoproteins and alfa-amin nitrogen were increased in comparison to the blood serum of control rats.

Alanine Transaminase↗
PubMed1998

Congenital infantile fibrosarcoma: a case study.

Congenital infantile fibrosarcoma (CIFS) is a rare soft-tissue malignancy most commonly involving the extremities. Metastases are rare; however, local recurrence is common. Because the tumor is so rare and clinical experience is lacking, both diagnosis and treatment are difficult. The complex planning and implementation of neonatal and oncologic care require ongoing collaboration between both nursing specialties. This case study discusses the pathophysiology, diagnosis, and management of an infant with CIFS, with emphasis on the nursing care of the patient and family.

Female↗
PubMed1998

A fibrosarcoma in a Siamese crocodile (Crocodylus siamensis).

A fibrosarcoma of periosteal origin was identified in the oral cavity of a 22-yr-old male captive Siamese crocodile (Crocodylus siamensis). The diagnosis was based upon the gross and light microscopical examination. The mesenchymal histogenesis was derived from the capability of the cells to produce collagen fibers. The invasive growth and the polymorphous cells in combination with the low mitotic index suggest a low-order malignancy. Attempts by immunohistochemical staining techniques to identify the specific lineage of the neoplastic cells and the expressed collagen type were unsuccessful.

Alligators and Crocodiles↗
PubMed1976

[Fibrosarcoma of the orbit (author's transl)].

During a period of 8 months a capsulated orbital tumour--not adherent the orbital walls or the bulbus--developed in a 21-year-old female patient. The tumour was exstirpated in toto. The histological findings show a fibrosarcoma with poorly differentiated cells, giant cells and numerous mitoses. The comparatively small incidence of the tumour as well as the prognosis quoad vitam are discussed.

Adult↗
PubMed1998

Dexamethasone up-regulates cadherin expression and cohesion of HT-1080 human fibrosarcoma cells.

The synthetic glucocorticoid dexamethasone markedly decreases the invasiveness of HT-1080 human fibrosarcoma cells. We show here that dexamethasone treatment of HT-1080 cell aggregates more than doubles their cohesivity from 3.9 to 9.7 dyne/cm. Western blot analysis shows a corresponding increase in cadherin expression. This was accompanied by an increase in the rate of calcium-dependent aggregation. Dexamethasone-treated aggregates spread to form a monolayer in Matrigel spreading assays, but the cells remained much more contiguous than their untreated counterparts. Invasion-suppression by dexamethasone may therefore be due, at least in part, to a previously unsuspected increase in cadherin-mediated cohesion.

Antineoplastic Agents, Hormonal↗
PubMed1976

Kinetics of the plasmacellular reaction in the draining lymph node of mice bearing the BP-8 fibrosarcoma.

The kinetics of the plasmacellular response in the draining lymph node was quantitatively assessed in specific-pathogen-free C3H/He mice grafted S.C. with the syngeneic BP-8 fibrosarcoma. The percentage of plasma cells was estimated on dissociated, cytocentrifuged, and fixed cell preparations by immunoenzymatic staining with either of two B-cell-specific antibody markers. Mice either grafted with liver tumor or given a single implant of tumor homogenate gave a maximal plasma cell response of about 4%. However, this peak was reached at 14 days in the live grafts and at 7 days in the homogenate situations. Moreover, in animals grafted with live tumor an elevated 3% plateau persisted until death, wheras in homogenate-implanted animals a sharp drop to a 0.5% plateau was observed at about Day 20. Homogenate-treated animals displayed a significant enhancement of tumor growth when challenged with a live graft 7 days after homogenate implantation, i.e., during the peak 4% plasmacellular response. Mice given a single implant of X-irradiated (3500 R) tumor responded with a peak of 1.7% plasma cells at 7 days. Despite subsequent boosting with the same material (Days 14 and 21), this value declined and remained at a plateau of about 0.2% until death. Contrary to homogenate-treated mice, these animals were immune to subsequent challenge with a live tumor graft. In the present host-tumor system, there appears to be an inverse relationship between elevated numbers of plasma cells and antitumor immunity.

Animals↗
PubMed1998

[A rare case of multiple primary malignant neoplasms of parotid gland: fibrosarcoma and squamous cell carcinoma].

Primary multiple malignant neoplasms and multifocal neoplasms are a very complex problem and therefore have been a topic of many articles. The mechanism of origin, frequency of occurrence, co-existence of neoplasms in functionally similar organs (uterus, mammary gland), heredity, a possibility of diagnostic and therapy are the most interesting aspects. Frequency of multiple primary malignant neoplasms occurrence is about 2-8% and still increases. Pathogenesis of multifocal and multiple neoplasms has rarely been a subject of articles. A simultaneous exposure of a tissue to damaging factors and special tissue sensitivity are the main reasons for neoplasms origin in this group. The authors present a rare case of parotid gland multiple neoplasm: fibrosarcoma and squamous cell carcinoma, as well as discuss the diagnostics, therapy, and prognosis of multiple neoplasms.

Antineoplastic Agents↗
PubMed1998

Gene transfer in dendritic cells, induced by oral DNA vaccination with Salmonella typhimurium, results in protective immunity against a murine fibrosarcoma.

A live attenuated AroA- auxotrophic mutant of Salmonella typhimurium (SL7207) has been used as carrier for the pCMVbeta vector that contains the beta-galactosidase (beta-gal) gene under the control of the immediate early promoter of Cytomegalovirus (CMV). We tested whether orally administered bacterial carrier could enter and deliver the transgene to antigen-presenting cells (APCs) through the natural enteric route of infection and whether beta-gal expression could generate a protective response against an aggressive murine fibrosarcoma transduced with the beta-gal gene (F1.A11) that behaves operationally as a tumor-associated antigen. After three courses, at 15-day intervals, mice developed both cell-mediated and systemic humoral responses to beta-gal. Mice vaccinated with the Salmonella harboring pCMVbeta, but not with plasmid-less carrier, showed resistance to a challenge with F1.A11 cells. These experiments suggest that Salmonella-based DNA immunization allows us to specifically target antigen expression in vivo to APCs. To prove that the transgene is actually expressed by APCs as a function of an eukaryotic promoter, the green fluorescent protein (GFP) was placed under the control of either the eukariotic CMV or a prokaryotic promoter. Using cytofluorometric analysis, GFP was detected only in splenocytes of mice receiving a Salmonella carrier harboring GFP under the CMV promoter. These results indicate that transgene expression occurs because of a Salmonella-mediated gene transfer to eukaryotic cells. Finally, approximately 19% of the splenocytes expressed GFP. Among them, F4/80(+) macrophages and CD11cbright dendritic cells (DCs) were scored as positive for GFP expression. Extensive work has been performed trying to optimize the way to transfect DCs, ex vivo, with genes coding for relevant antigens. We show here, for the first time, that DCs can be directly and specifically transduced in vivo such to induce DNA vaccination against tumors.

Administration, Oral↗
PubMedDate not supplied

[Undifferentiated pelvic fibrosarcoma. A new case report].

Genitourinary sarcomas are very rare entities. This paper contributes one case report of an undifferentiated pelvic fibrosarcoma in a 53-year old patient. It also includes some observations on the clinical development, complementary studies used, difficulties for the pathoanatomical diagnosis and treatment issues.

Diabetes Mellitus, Type 2↗
PubMed1998

ETV6-NTRK3 gene fusions and trisomy 11 establish a histogenetic link between mesoblastic nephroma and congenital fibrosarcoma.

Congenital mesoblastic nephroma (CMN) is an infantile spindle cell tumor of the kidney that is subdivided into "classical" and "cellular" forms based on the degree of cellularity and mitotic activity. The histogenesis of CMN remains obscure, but relationships to other pediatric renal neoplasms have been proposed. However, cellular CMN is virtually identical histologically to congenital fibrosarcoma (CFS), a malignant tumor of fibroblasts in children of the same age group. Moreover, cytogenetic studies have reported common trisomies in CFS and cellular CMN, particularly of chromosome 11. We show here that t(12;15)(p13;q25)-associated ETV6-NTRK3 gene fusions described in CFS are also present in cellular CMN. ETV6-NTRK3 chimeric transcripts were detected in 8 of 9 cellular CMNs and 2 of 2 mixed CMNs. In contrast, all of the four classical CMNs tested were negative, as were cases of Wilms' tumor and clear cell sarcoma of the kidney. Moreover, we found trisomy 11 only in cellular or mixed CMNs with the ETV6-NTRK3 gene fusion. Our studies indicate that classical and cellular CMN have different genetic features and support the concept that cellular CMN is histogenetically related to CFS. They also provide insight into potential mechanisms involved in the transformation of the classical into the cellular form of CMN.

Child, Preschool↗
PubMed1976

The effect of 1-beta-D-arabinofuranosylcytosine on cell viability, DNA synthesis, and chromatid breakage in synchronized hamster fibrosarcoma cells.

Hamster fibrosarcoma cells were synchronized by mitotic selection and exposed to varying concentrations of 1-beta-D-arabinofuranosylcytosine (ara-C) for 2 hr in mid-S phase. There was a direct relationship between DNA synthesis inhibition and cytotoxicity produced by ara-C once DNA synthesis was decreased by over 85%. The noncytotoxic concentration of 10(-5) M ara-C produced little chromatid breakage; but extensive chromatid breakage and chromosomal rearrangement were seen in cells treated with the cytotoxic concentration of 10(-3) M ara-C, thus supporting earlier observations that chromatid breakage is highly correlated with cytotoxicity. Predominantly small DNA was synthesized when cells were treated with both 10(-5) and 10(-3) M ara-C, and this DNA could be completely chased into high-molecular-weight DNA after addition of deoxycytidine. Both concentrations of ara-C also inhibited, to different degrees, the joining of intermediate-size DNA fragments into larger DNA; thus neither parameter appeared directly related to the ara-C-produced cytotoxicity.

Animals↗