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PubMed2001

[Rare case of multiple primary malignant neoplasm of the larynx: squamous carcinoma and fibrosarcoma].

The problem of primary mixed neoplasms has been recently a subject of numerous research works trying to find out their pathogenetic mechanisms, early detection, clinical course and treatment opportunities. The authors present a rare case (fibrosarcoma and squamous carcinoma) in a 73-year-old man. The patient had a surgery (total laryngectomy) and complementary irradiation at the Institute of Oncology.

Aged↗
PubMed1992

Molecular analysis of the inhibition of interleukin-8 production by dexamethasone in a human fibrosarcoma cell line.

In order to analyse the effects of glucocorticoids on interleukin-8 (IL-8) production more precisely, we examined the effects of dexamethasone on IL-8 production at the molecular level in a human fibrosarcoma cell line, 8387, which IL-1 induces to express IL-8 messenger RNA (mRNA) and to secrete IL-8. Over a wide dose range, dexamethasone inhibited IL-8 production induced by IL-1 alpha stimulation. Northern blotting analysis showed that dexamethasone also inhibited the IL-8 mRNA accumulation in a similar dose-related manner. Nuclear run-off assay revealed that dexamethasone decreased the transcription of the IL-8 gene and the degree of inhibition of transcription correlated well with the inhibition of IL-8 production, suggesting that the action of glucocorticoids is mainly at the transcriptional level. Furthermore, transfection with chloramphenicol acetyl transferase (CAT) expression vectors inserted with the 5'-deleted IL-8 gene demonstrated that the 5'-flanking region which contains the glucocorticoid response element (GRE) was mainly involved in the dexamethasone-induced repression of the IL-8 gene. These data suggest that the inhibition of the IL-8 gene transcription by glucocorticoids occurs through the interaction of the glucocorticoid receptor complex with GRE in the 5'-flanking region of the IL-8 gene.

Blotting, Northern↗
PubMed2005

[Effect of calmodulin antagonist EBB on invasion of human fibrosarcoma cell HT1080].

OBJECTIVE: To investigate the potential effect of EBB, a calmodulin antagonist, on invasion of human fibrosarcoma cells HT1080. METHODS: The antitumor effect of EBB was assessed by 3-(4,5-Dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium bromide (MTT) assay. Activities of matrix metalloproteinase (MMP)-2 and MMP-9 were measured by Zymogrophy analysis. The mRNA levels, of MMP-2, MMP-9, and tissue inhibitor of metalloproteinases (TIMP)-1 were evaluated by reverse transcriptionpolymerase chain reaction (RT-PCR). Transwell chamber assay was applied to measure the effect of EBB on the invasion of HT1080 cells. RESULTS: Calmodulin antagonist EBB inhibited the proliferation of HT1080 cells with an IC50 of (8.2 +/- 1.2) microg/ml. EBB down-regulated the activities of MMP-2 and MMP-9, and down-regulated the mRNA levels of MMP-2 and MMP-9, while up-regulated the mRNA levels of TIMP-1. The invasive ability of HT1080 cells was decreased to (31.13 +/- 2.265)%, (59.91 +/- 2.566)%, and (71.58 +/- 0.5960)% after exposure of the cells with 2, 5, and 10 microg/ml EBB, respectively. CONCLUSION: Treatment with calmodulin antagonist EBB is effective in suppressing tumor invasion. The possible mechanism is the down-regulation of MMPs.

Antineoplastic Agents↗
PubMed1992

[Extrapancreatic hypoglycemic tumors. Apropos of a case of pleural fibrosarcoma].

The authors report a case of pleural fibrosarcoma associated with severe hypoglycaemia. Chromatography of the patient's serum and tumour fragments revealed a substance with a high molecular weight and an insulin-like activity. Professor Poffengarger's laboratory identified this substance as Non Suppressible Insulin-Like Protein or NSILAp which induces insulin-like effects on various tissues. A review of the literature is presented in the light of this case.

Adult↗
PubMedDate not supplied

Response of subpopulations of the FSall C fibrosarcoma to low dose x-rays and various potential enhancing agents.

The effectiveness of various oxygen carrying treatments in sensitizing subpopulations of the FSallC fibrosarcoma to low doses of radiation was assessed, and compared with survivals obtained with the same cells after in vivo irradiation under normally oxygenated or hypoxic conditions. FSallC tumors were treated with 2-10 Gray then the Hoechst 33342 dye diffusion method was used to separate the tumor into bright (enriched in normally oxygenated cells) and dim (enriched in hypoxic cells) subpopulations. There was good agreement between the survival of normally oxygenated cells in culture and bright cells from tumors and between hypoxic cells in culture and dim cells from tumors over a radiation dosage range of 2-5 Gray. At 10 Gray bright cells from tumors were minimally less sensitive to the radiation dose than normally oxygenated cells in vivo. When maximally effective doses of perfluorochemical emulsions (F44E at 4 g PFC/kg or Fluosol-DA at 2.4 g PFC/kg) or a purified bovine hemoglobin solution (PBHS at 1.32 g protein/kg) were administered 1 hr. prior to radiation therapy with carbogen (95% O2, 5% CO2) breathing prior to and during radiation delivery, low single doses of x-ray (2-5 Gray) were measurably more cytotoxic toward both FSallC tumor cell subpopulations. These results indicate that perfluorochemical emulsions or purified bovine hemoglobin preparations along with carbogen breathing may be able to increase tumor radiosensitivity to the relatively low radiation doses per fraction used in the clinic.

Animals↗
PubMed2005

Indication of a role of plasminogen activator inhibitor type I in protecting murine fibrosarcoma cells against apoptosis.

In a number of cancer types high tumor tissue levels of plasminogen activator inhibitor type 1 (PAI-1) protein are strongly associated with shorter cancer patient survival. This association has been intriguing since PAI-1 is known to inhibit urokinase plasminogen activator (uPA) that converts plasminogen to plasmin, which is actively involved in tumor progression and invasion. In order to further explore the biological role of PAI-1 in cancer, we have prepared fibroblasts from PAI-1 gene deficient mice and from their wild type littermates. From these fibroblasts fibrosarcoma cell lines were established and characterized. Both types of fibroblasts underwent spontaneous transformation as indicated by aneuploidy, immortalization, clonogenicity in soft agar and tumor formation in vivo. While both PAI-1 deficient and PAI-1 expressing cell lines showed similar proliferation rates in vitro, cells devoid of PAI-1 were significantly more sensitive to apoptotic stimuli. When inoculated subcutaneously into nude mice PAI-1 expressing cells rapidly established tumors, while PAI-1 deficient cells had a significantly longer lag-phase before they started to grow (p<0.0001). The present study suggests that PAI-1, besides its uPA inhibiting function, has a role in cancer progression by protecting tumor cells from undergoing apoptosis.

Animals↗
PubMed1990

Incapacitation of fibrosarcoma cell by polyclonally activated murine T cell.

A piece of lymph node containing polyclonally-activated lymphocytes when transplanted in the anterior eye chamber of mouse along with solid piece of fibrosarcoma from syngeneic Swiss mice, dramatically inhibited the tumour-induced-vasodilatation and neo-vascularization. If the tumour explants were incubated in vitro with activated lymphocytes prior to transplantation, such angiogenic reactions was significantly reduced. These explants were incapable of incorporating radioactive thymidine in vitro. Furthermore, the cytotoxic ability of activated lymphocytes towards 51Cr labelled tumour target cells was of significant level indicating the possible mechanism of immunological reactiveness of Con A-stimulated lymphocytes to 3'-methylcholanthrene-induced tumour cells of syngeneic origin.

Animals↗
PubMed1991

Resistance to NK and metastatic potential of fibrosarcoma cells is associated with products encoded by the H-2D region.

We have used the murine 3-methylcholanthrene induced T10 fibrosarcoma tumor cell system originating in (C3II/en x C57BL/6)F1 mice (H-2b x H-2k) to elucidate the possible correlation between metastatic potential, expression of individual H-2 antigens and susceptibility to NK cells. Transfection of the non metastatic and NK sensitive IC9 cells (Db+, Kk, Kb, Kk-) with the H-2Dk gene, altered the metastatic phenotype of the parental cells, yet had no effect on the susceptibility of these tumor cells to lysis by NK and did not elicit a specific CTL response in syngeneic hosts. Variants of the metastatic and NK resistant IE7 clone (Db+, Kk-, Kb-, Kk-), lacking H-2Dk, were selected by treatment with monoclonal anti H-2Dk antibodies and complement. These variants were sensitive to NK and poorly or non metastatic. Transfection of Dk negative variants with the H-2Dk gene, resulted in the isolation of several clones which expressed a wide range of metastatic phenotypes but maintained sensitivity to NK. In addition, by cloning the cDNA of the H-2Dk gene of the metastatic T10-IE7 variant cells and analyzing its nucleotide sequence, we found four single nucleotide changes. Two of them are not expected to alter the encoded amino acids, whereas the others should result in two amino acid substitutions in the alpha-2 domain of the class I H-2Kd protein product. These changes might account, at least partially, for the failure of the transfection of H-2Dk to restore resistance to NK.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Collagenolytic activity of methylcholanthrene-induced rat fibrosarcoma.

It has been found that the methylcholanthrene-induced rat fibrosarcoma contains an enzyme (probably a cathepsin) which digests type I and type III collagens in acid pH. At physiological pH no proteolytic activity against collagen was found. It may be concluded that the tumour collagen is degraded mainly by the action of cathepsin(s).

Animals↗
PubMed1991

Modulation of alkylating agents by etanidazole and Fluosol-DA/carbogen in the FSaIIC fibrosarcoma and EMT6 mammary carcinoma.

Tumor cell survival assay in the FSaIIC murine fibrosarcoma demonstrated that when the modulator Fluosol-DA (0.3 ml; 12 ml/kg i.v.) was administered just prior to an alkylating agent plus carbogen breathing for 6 h or the modulator etanidazole (1 g/kg i.p.) was administered just prior to an alkylating agent, the combination treatment produced significantly more tumor cell killing across the dosage range of each alkylating agent tested compared with the alkylating agent alone. Each alkylating agent produced a dose-dependent log-linear tumor cell survival curve. There was an increase in tumor cell killing of 5-10-fold when either Fluosol-DA/carbogen or etanidazole was added to treatment with the alkylating agent. For cis-diamminedichloroplatinum(II) (CDDP) and N,N',N''-triethylenethiophosphoramide, the modulators used in combination increased tumor cell killing by only 2-3-fold over that obtained with a single modulator, but for the other alkylating agents, tumor cell killing was increased by 10-50-fold when the combination of modulators was used. Bone marrow granulocyte-macrophage colony-forming unit survival assays showed that the combination of modulators with the alkylating agents resulted in only small increases in bone marrow toxicity of the alkylating agents except for N,N',N''-triethylenethiophosphoramide and L-phenylalanine mustard (L-PAM), for which the toxicity to the bone marrow granulocyte-macrophage colony-forming unit was increased by 5-10-fold compared with the alkylating agents alone. The Hoechst 33342 dye diffusion defined tumor cell subpopulation assay, also in the FSaIIC tumor, demonstrated that the combination of modulators increased the toxicity of CDDP, cyclophosphamide, L-PAM, and 1,3-bis(2-chloroethyl)-1-nitrosourea by 9-55-fold compared with the alkylating agent alone in both the bright (euxoic-enriched) and dim (hypoxic-enriched) cells. For each alkylating agent except 1,3-bis(2-chloroethyl)-1-nitrosourea, the increase in tumor cell killing was greater in the dim cells than in the bright cells. Finally, tumor growth delay studies in both the FSaIIC tumor and the EMT-6 murine mammary adenocarcinoma confirmed that the combination of modulators significantly increased the tumor growth delay caused by CDDP, carboplatin, cyclophosphamide, N,N'N"-triethylenethiophosphoramide, L-PAM, and 1,3-bis(2-chloroethyl)-1-nitrosourea. The greatest increases (4-5-fold) were observed for carboplatin and L-PAM in the FSaIIC tumor and CDDP and cyclophosphamide in the EMT-6 tumor. These results suggest that Fluosol-DA/carbogen together with etanidazole may be an effective modulator combination of alkylating agents in the clinic.

Alkylating Agents↗
PubMed1991

Immunoelectron microscopic localization of the p21 protein in HT1080 human fibrosarcoma cell lines with altered N-ras gene expression.

The cellular localization of the p21 protein was studied by immunoelectron microscopy in human fibrosarcoma cells with different N-ras gene expression. The tumorigenic HT1080 cells--expressing equally the normal and mutant N-ras genes--contained the p21 in the plasma membrane, in pinocytotic areas as well as in the intracellular vesicles. The non-tumorigenic revertants--expressing more normal N-ras gene than the mutant one--contained p21 in the plasma membrane, especially at the cell junctions. These results suggest, that the mutant p21 may locate to the membrane areas connected with pino- or endocytotic functions.

Fibrosarcoma↗
PubMed1991

Immunoelectron microscopic localization of the p21 protein in HT1080 human fibrosarcoma cell lines with altered N-ras gene expression.

The cellular localization of the p21 protein was studied by immunoelectron microscopy in human fibrosarcoma cells with different N-ras gene expression. The tumorigenic HT1080 cells-expressing equally the normal and mutant N-ras genes-contained the p21 in the plasma membrane, in pinocytotic areas as well as in the intracellular vesicles. The non-tumorigenic revertants-expressing more normal N-ras gene than the mutant one-contained p21 in the plasma membrane, especially at the cell junctions. These results suggest, that the mutant p21 may locate to the membrane areas connected with pino- or endocytotic functions.

Cell Division↗
PubMed1991

Interleukin-2 and syngeneic bone marrow transplantation in a murine fibrosarcoma model.

Mice received interleukin-2 (IL-2) either before and after, or just after intravenous inoculation of syngeneic fibrosarcoma cells. Fewer pulmonary tumor colonies were observed in those animals treated with IL-2, and the best results were observed when IL-2 was administered prior to tumor inoculation. When mice were lethally irradiated and reconstituted with tumor-contaminated bone marrow, IL-2 treatment was also associated with fewer tumor lung colonies. IL-2 may prove to be a useful adjuvant therapy, particularly in the setting of autologous bone marrow transplantation when the infused marrow is contaminated with tumor cells.

Animals↗
PubMed1991

Modulation of murine radiation-induced fibrosarcoma-1 tumor metabolism and blood flow in situ via glucose and mannitol administration monitored by 31P and 2H nuclear magnetic resonance spectroscopy.

The hyperglycemia-induced in situ metabolism and blood flow changes produced in s.c. implanted murine radiation-induced fibrosarcoma-1 tumors, grown on the flanks of female C3H/HeJ mice, were examined with 31P and 2H nuclear magnetic resonance. Initial experiments verified a hyperglycemic tumor acidification similar to that reported earlier with a different substrain of mice, C3H/AnF (J.L. Evelhoch et al., Proc. Natl. Acad. Sci. USA, 81: 6496-6500, 1984). Changes in the tumor pH, phosphorus metabolites, and blood flow were then compared after administration of saline, glucose, or mannitol (a nonmetabolizable glucose analogue) using a mole-equivalent dose of the sugars (i.e., 0.8 mmol/20g mouse). Neither saline (n = 8) nor mannitol (n = 6) administration had any marked effect upon tumor pH, whereas glucose administration produced a mean maximum tumor pH reduction of 0.74 +/- 0.09 (SE; n = 9) during the 2.5 h post-glucose injection. No significant changes in high energy phosphate concentrations were observed during the same period after saline injection. After glucose injection, the [phosphocreatine] gradually decreased by 64% (P = 0.0001). After the initial 1 h post-glucose injection, the [inorganic phosphate] increased by 58% (P = 0.0001), and the [nucleoside triphosphates] decreased by 29% (P = 0.0001) during the following 1.5 h. After mannitol injection, while there was no change in [inorganic phosphate] over time (P = 0.37), the [phosphocreatine] decreased by 33% (P = 0.0001) and the [nucleoside triphosphates] decreased by 21% (P = 0.0015) within 20 min, then both the [phosphocreatine] and [nucleoside triphosphates] remained at constant levels during the following 2 h. In parallel experiments, the volumetric rate of tumor blood flow and perfusion was measured by 2H nuclear magnetic resonance monitoring of 2H2O washout kinetics (S-G. Kim and J. J. H. Ackerman, Cancer Res., 48: 3449-3453, 1988); tumor blood flow decreased by 80% (P = 0.0001, n = 11), 60% (P = 0.0031, n = 4), and 20% (P = 0.058, n = 10) at 2 h after glucose, mannitol, or saline injections, respectively. These results suggest that anaerobic glycolysis is a requirement for hyperglycemic tumor acidification. However, the decrease in tumor blood flow accompanying hyperglycemic acidification suggests that flow reduction also may be a contributing or a required cofactor for acidification via inhibition of lactic acid egress.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1977

Radiation-induced fibrosarcoma following treatment for breast cancer.

A patient with radiation-induced fibrosarcoma following mastectomy and postoperative radiation for bilateral breast carcinoma is described. Only six such cases have been reported in the literature. In this patient erosion of the axillary artery produced massive hemorrhage, and emergency transthoracic ligation of the subclavian artery caused gangrene of the extremity and empyema and sepsis. Interscapulothoracic amputation not only was life-saving but offered the patient a reasonable chance for long-term survival. Only aggressive surgical management can salvage a patient with radiation-induced sarcoma.

Breast Neoplasms↗
PubMed1991

Frequent p53 mutations in chemically induced murine fibrosarcoma.

Patterns of p53 expression were investigated in chemically induced fibrosarcoma tumors and cell lines. Most, if not all, cell lines were found to carry alterations at the protein level, reflected in the overproduction of greatly stabilized p53 proteins. In many cases, this was accompanied by formation of complexes with hsc70. Hence, all of these lines may be expressing one sort or another of mutant p53. The mutant nature of the p53 gene was directly verified, in a number of cases, by PCR-amplified cDNA cloning. In one line, no p53 protein was made at all; this turned out to be because of a mutation in a splice donor site, resulting in the production of an aberrant mRNA. In all other cases, mRNAs carrying mis-sense mutations were present, and were sometimes expressed along with wt p53 mRNA. When tested in an in vitro transformation assay, all cloned mutants possessed a discrete oncogenic activity, while having lost the ability to interfere with oncogene-mediated transformation. The system described here could potentially be very helpful in elucidating the significance of p53 mutations.

Animals↗
PubMed1991

The development of a treatment model for lymph node metastasis in nude mice transplanted with rat fibrosarcoma clone A.

We have tried to establish a model for lymph node metastasis in nude mice transplanted with clone A of methylcholanthrene-induced rat fibrosarcoma. Tumor cells transplanted either subcutaneously or intrafootpad metastasized exclusively to the lymph nodes in nude mice treated with antiasialo GM1 antiserum. In the experiments of intrafootpad transplantation, all the mice died of disseminated lymph node metastasis if the leg was not resected, or was resected more than 3 weeks after the transplantation of clone A. Some mice whose legs were amputated 1 or 2 weeks after transplantation could be cured by amputation alone. The maximum effective dose of in vitro active drug could improve the survival in mice, and 3/5, 4/5, and 3/5 mice treated with MMC, ACNU and CDDP respectively were cured even if their legs were amputated 3 weeks after transplantation. This tumor-bearing animal system was considered to provide a valuable experimental model for lymph node metastasis.

Amputation, Surgical↗