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PubMedDate not supplied

Phorbol ester binding and phorbol ester-induced arachidonic acid metabolism in a highly responsive murine fibrosarcoma cell line and in a less-responsive variant.

Phorbol ester binding was examined in two lines of murine fibrosarcoma cells. The two cell lines were isolated from the same parent tumor but respond differentially to stimulation with phorbol esters. In one of the lines, these agents stimulate a rapid attachment and spreading response and induce directional migration. The other cell line does not migrate in response to stimulation with phorbol esters and the attachment and spreading response is slow. The cell line which responds actively to phorbol ester stimulation is highly malignant when injected into syngeneic animals while the other line is of low tumorigenicity and is virtually non-metastatic. In spite of these differences, both lines were found in the present study to bind [3H]4 beta-phorbol-12 beta, 13 alpha-dibutyrate in a receptor-mediated fashion. The characteristics of binding were virtually identical between the two cell lines. In additional studies, arachidonic acid metabolism was examined in the same two lines. In the highly responsive line, PMA stimulated a rapid release of [3H]arachidonic acid and its conversion into cyclooxygenase and lipoxygenase products. In the less-responsive line, PMA stimulated a slower release of [3H]arachidonic acid from prelabeled cells. The quantity of arachidonic acid metabolites produced was also much less. These studies suggest that the disparity between the two cell lines in their response to phorbol ester stimulation is not the result of differences in the initial interaction between the cells and ligand but may result from alterations in their signal transductance mechanism. This may be the result of inherent differences in capacity for arachidonic acid metabolism.

Animals↗
PubMed1993

Antimetastatic activity of lipopolysaccharide against a NK-resistant murine fibrosarcoma.

An intravenous injection of bacterial lipopolysaccharide (LPS) into mice exerted prominent antimetastatic activities against a NK-resistant weakly immunogenic NFSa fibrosarcoma. The number of visible metastases in the lung was increased by a pretreatment of anti-asialoGM1 (asGM1) antibody or silica, but pretreatment of asGM1 antibody or silica scarcely affected the antimetastatic activities of LPS. The pulmonary retention of radiolabeled tumor cells showed that LPS accelerated the detachment of the tumor cells from the lung, and that this acceleration was not suppressed by anti-asGM1 antibody. Sialic acids of lung endothelial cell surface, essential components of various receptors, was diminished by the i.v. injection of LPS. These results suggested that the antimetastatic effect of LPS against NK-resistant NFSa cells was partly the result of modulations of lung endothelial cell surface.

Animals↗
PubMed1992

Calcium depletion reduces the destruction of fibrosarcoma cells in the microvasculature of artificially perfused rat hearts.

Earlier studies have shown that most tumour cells (TCs) injected into the circulation die rapidly. The mechanisms behind this rapid elimination of TCs are not known, but some experimental data suggest that mechanical trauma to the cells in the capillary bed plays a role. In the present investigation 725,000 rat fibrosarcoma cells (250,000/ml) were infused into the coronary microcirculation of isolated and artificially perfused (flow rate approx. 6 ml/min), beating and non-beating (Ca2+ excluded from the perfusate) rat hearts. The analyses included calculations of the number of TCs retained in the myocardium 5 min after start of TC infusion and their distribution within the ventricular wall. In addition, ultrastructural studies were performed to identify possible structural changes of trapped TCs and myocardial tissue. Intact and viable TCs in the effluent perfusate were counted. In beating hearts about 20% of the infused TCs were collected microscopically intact after passage through the heart circulation, and of these cells only 32% were viable (in-flow viability 87-91%). In Ca(2+)-depleted hearts the corresponding figures were 29 and 48%, respectively. The difference in viable cell counts was statistically significant (P less than 0.001). The TCs trapped in the left ventricular wall of the myocardium of beating hearts were mainly found in the subepicardial third of the wall, whereas in non-beating hearts the trapped cells were distributed randomly. The ultrastructural appearance of trapped cells differed between the two groups: 82% of cells trapped in beating hearts showed signs of severe damage, with subcellular vacuolization and plasmalemmal disruption, whereas 65% of cells trapped in Ca(2+)-depleted hearts seemed undamaged with intact cell membranes and cytoplasmic organization. The remaining 35% showed variable subcellular disorganization. The results cannot entirely be explained by mechanical TC damage in the microcirculation due to intracapillary deformation. The observations require additional explanatory mechanisms. One possible important TC damaging mechanism, dependent on extracellular Ca2+ levels, could be endothelial cell release of reactive oxygen species.

Animals↗
PubMedDate not supplied

Invasiveness and tumorigenicity of MO4 mouse fibrosarcoma cells pretreated with microtubule inhibitors.

MO4 cell aggregates with a diameter of 0.3 mm produced invasive fibrosarcomas after s.c. implantation into the pinna of syngeneic mice. Histology of pinnae fixed 10 min to 5 days after implantation of an aggregate suggested that the tumour was produced by the cells that invaded during the first day, and that the cells remaining in the aggregate were eliminated by the reaction of the host. Before implantation we have pretreated MO4 cell aggregates with 1 microgram/ml of the microtubule inhibitors Nocodazole (ND) and vincristine (VCR), known to inhibit both proliferation and invasion, and with 1 microgram/ml 5-fluorouracil (5-FU), known to inhibit proliferation but not invasion. Tumorigenicity was significantly reduced after treatment with ND or VCR, as compared to treatment with 5-FU or to controls. Histology of pinnae fixed 10 min to 3 days after implantation showed absence or scarceness of invasive MO4 cells after pretreatment with ND or VCR, in contrast with controls or with aggregates pretreated with 5-FU. The effect of ND, VCR and 5-FU on the growth of aggregates in culture on gyrotory shaker was reversible within 1 and 2 days respectively. After treatment with ND or VCR slight alterations in the function of the cytoplasmic microtubule complex remained visible during 3 days in cells migrating from an aggregate explanted on glass. Confrontation of pretreated aggregates with fragments of embryonic chick cardiac muscle in three-dimensional culture indicated that the anti-invasive effect of ND or VCR was reversible in vitro. We concluded that a delay of invasiveness caused by pretreatment with ND or VCR provided the host with the opportunity to eliminate MO4 cells implanted s.c. into the pinna.

Animals↗
PubMedDate not supplied

Proteolytic and metastatic activities of clones derived from a methylcholanthrene-induced murine fibrosarcoma.

Eighteen clones of a methylcholanthrene-induced murine fibrosarcoma (3AM) which were heterogeneous with respect to metastatic potentials and in vivo growth rates were examined for five different protease activities: acid protease (cathepsin D), BANA hydrolase (cathepsin B), neutral protease, collagenase, and plasminogen activator. Homogenates of the solid tumors produced by the clones were heterogeneous with respect to the activities of the proteases; these activities were in all cases (except plasminogen activator) higher than those obtained for normal muscle tissue. There was, however, no correlation between any of these protease activities and the metastatic potential or in vivo growth rates. The cathepsin B activity has also been evaluated on the cultured cells of the various clones. Results similar to that of the in vivo study were obtained. Analysis of the enzyme activity of the cell culture and of organ culture media, however, revealed no cathepsin B activity. It is concluded that the measurement of any one biochemical parameter such as proteolysis may not be sufficient to establish a correlation with the overall process of metastasis; a more precise dissection of the individual steps culminating in metastasis may provide a more fruitful approach to this problem.

Aminopeptidases↗
PubMed1992

YIGSR, a synthetic laminin peptide, inhibits the enhancement by cyclophosphamide of experimental lung metastasis of human fibrosarcoma cells.

Tumor cells must attach themselves to basement membranes, through which they degrade and migrate, in order to spread to distant sites. If vascular endothelial cells are damaged by pretreatment with anticancer drugs and the subendothelial basement membranes are exposed, the attachment of malignant cells to basement membranes and subsequent metastasis formation in some tissues may be enhanced. In this study, the pretreatment of endothelial cell monolayers and mice with cyclophosphamide (CPA) was respectively shown to promote the adhesion of HT1080 human fibrosarcoma cells to endothelial cell monolayers in vitro and lung colonization in vivo. YIGSR, a synthetic laminin pentapeptide, inhibited the enhancement of lung colonization by CPA when it was co-injected intravenously with tumor cells. This inhibitory effect of YIGSR may be due to a reduction in the adhesion of HT1080 cells to injured blood vessel walls since YIGSR inhibited both the adhesion of HT1080 cells to CPA-treated endothelial cell monolayers and the invasion through basement membranes in vitro.

Animals↗
PubMedDate not supplied

Effectiveness of AMSA alone or in combination with radiation on murine fibrosarcoma pulmonary nodules.

The cytotoxic effects in vivo of 4'-(9-acridinylamino) methanesulfon-m-anisidide (AMSA), radiation or both modalities in combination on murine fibrosarcoma (FSa) cells grown as pulmonary tumors were determined. Fourteen days following the i.v. injection of viable FSa cells, recipient mice developed between 100 and 150 visible pulmonary nodules. At that time, tumor-bearing animals were exposed to either single or combined modality treatments, as well as single and fractionated dose regimens. Animals were sacrificed 1 hour after the last treatment. Tumor nodules were excised, made into a single cell suspension and separated on the basis of cell size by centrifugal elutriation. Flow microfluorometry (FMF) was used to determine the cell-cycle parameters and the relative synchrony of the separated populations, as well as the percentage contamination by normal diploid cells in each of the tumor cell populations. Known numbers of viable cells from each elutriator fraction were injected into recipient mice to determine their colony-forming efficiency (CFE). Surviving fractions were determined by comparing the CFEs of treated FSa cells from each of the separated elutriator fractions with those of appropriate untreated controls. Following a single i.v. dose of AMSA (30 mg/kg), populations of cells enriched in S phase were the most sensitive. When a single dose of AMSA was combined with a single dose of radiation (100 rad), there was a marked schedule dependence with the more effective sequence, especially if a 12 hour interval was chosen between doses, being AMSA followed by irradiation. No schedule dependence was observed if both modalities were combined and administered under a fractionated protocol of four fractions of AMSA (5 mg/kg per fraction) and four fractions of radiation (300 rad per fraction). Under these conditions the greatest reduction in CFE was in cell subpopulations most enriched in S and G2 + M phase cells.

Aminoacridines↗
PubMedDate not supplied

Expression of a specific protein in spontaneously metastatic fibrosarcoma cell lines and its enhanced synthesis by growth on laminin or fibronectin.

A panel of tumor cell lines and clones was generated by selecting for different metastatic capacity in 3AM fibrosarcoma cells. These cell lines were exposed to substrata of various purified extracellular matrix (ECM) proteins and labeled in culture with [35S]methionine. Following analysis by two-dimensional polyacrylamide gel electrophoresis the profiles of total cellular proteins produced by the cell lines displaying different phenotypes were examined. The presence of a specific protein, p54, was related to the cellular metastatic potential, and the synthesis of p54 was influenced by growth on extracellular matrix components. The amount of p54 was minimal and non-inducible in tumor cell lines exhibiting two different phenotypes: (1) experimentally metastatic (EM) and (2) transformed, non-tumorigenic (NTT) cell types. In contrast, all of the five different cell lines capable of both spontaneous and experimental metastasis (SEM), produced p54 either constitutively or through induction by growth on ECM protein substrata of either laminin of fibronectin, but not collagen type IV. These data suggest that the p54 protein may be a unique biochemical marker associated with spontaneous metastatic cell types.

Animals↗
PubMed1991

A novel N-myristylated synthetic octapeptide inhibits protein kinase C activity and partially reverses murine fibrosarcoma cell resistance to adriamycin.

This report shows that N-acylation of the protein kinase C (PKC) substrate Arg-Lys-Arg-Thr-Leu-Arg-Arg-Leu (RKRTLRRL) provides it with a potent inhibitory activity against PKC. N-myristoyl-RKRTLRRL inhibited Ca2(+)- and phosphatidylserine (PS)-dependent histone phosphorylation catalyzed by PKC with a 50% inhibitory concentration (IC50) of 5 microM, whereas neither RKRTLRRL nor myristic acid inhibited PKC-catalyzed histone phosphorylation at concentrations as high as 50 microM. A fully active, Ca2(+)- and PS-independent catalytic fragment of PKC can be generated by limited proteolysis. N-myristoyl-RKRTLRRL inhibited histone phosphorylation catalyzed by the catalytic fragment of PKC (IC50 = 80 microM), but neither myristic acid nor the nonmyristylated peptide inhibited the activity of the catalytic fragment at concentrations up to and including 200 microM. The Km app and Vmax app for N-myristoyl-RKRTLRRL were similar to those of RKRTLRRL. Thus, N-myristylation provided the octapeptide with an inhibitory activity against PKC but had only minor effects on its Km app and Vmax app. Kinetic analysis provided evidence that the peptide inhibited PKC noncompetitively with respect to ATP. Previously, we reported that the protein kinase inhibitor H7 partially reverses Adriamycin resistance in the multidrug resistant (MDR) murine fibrosarcoma line UV-2237M-ADRR. In this report, we show that N-myristoyl-RKRTLRRL also partially reverses Adriamycin resistance in UV-2237M-ADRR cells. These results suggest that potent and selective cell permeable PKC inhibitors may be designed by N-acylating small PKC peptide substrates.

Amino Acid Sequence↗
PubMed1986

Development of highly immunogenic variants of a rat fibrosarcoma line during in vitro cultivation.

Rat fibrosarcoma KMT-17 cells decreased in tumorigenicity when cultured in vitro. Eight clones derived from cultured KMT-17 cell lines (c-KMT-17) were examined for their tumorigenicity, immunosensitivity, and immunogenicity. All the clones were less or nontumorigenic in normal syngeneic rats than KMT-17 cells maintained in vivo. All eight clones produced tumors in rats immunosuppressed with 600 rad 60Co; differences in degree of tumorigenicity were seen among clones in rats irradiated with 250 rad 60Co. Although immunosensitivity of the eight clones to complement-dependent and cell-mediated cytotoxicity was the same or less than that of KMT-17 cells, al leight clones induced greater transplantation resistance to KMT-17 than KMT-17 itself. Cold target inhibition tests demonstrated new antigens in a highly immunogenic variant in addition to the original tumor associated antigen (TAA). New glycolipids, not observed in KMT-17 cells, were demonstrated in the clones by thin layer chromatography. These results suggest that new antigens appearing during culture of KMT-17 may act as helper antigens for TAA, increasing the immunogenicity and decreasing the tumorigenicity of the cultured cells.

Animals↗
PubMed1988

Characterisation of suppressor cells generated following cryosurgery of an HSV-2-induced fibrosarcoma.

Cryosurgery of a primary HSV-2-induced hamster fibrosarcoma resulted in the generation of a population of suppressor cells. These cells were detectable in the spleen 1-10 days post-cryosurgery by their ability to suppress the proliferation of immunocompetent splenic T-lymphocytes following exposure to concanavalin A (Con A). The spleens of tumour-bearing (t.b.) animals which received cryosurgery 3 days previously displayed gross splenomegaly due to the generation of large numbers of highly proliferative erythroblasts. The erythroblast cells were unlikely to be the source of suppression since time course studies have demonstrated the presence of suppressor cells before and after their appearance in the spleen. The erythroblasts therefore probably reflected a response by the host to regenerate the erythrocytes lost during surgery and their presence was independent of the appearance of suppressor cells. Characterisation of the suppressor cell has revealed it to be non-adherent and esterase negative making it unlikely to be of macrophage (MO) lineage. This was confirmed by the ability of splenic MOs from day 3 t.b. cryosurgery-treated animals to completely restore Con A-dependent T-lymphocyte proliferation following MO depletion. As nylonwool column-eluted cells are able to suppress Con A-dependent T-lymphocyte proliferation, it seemed unlikely that B-lymphocytes play a role in cryosurgery-induced immunosuppression. These findings suggest that cryosurgery of a t.b. animal results in the generation of a population of T-lymphocytes capable of suppressing Con A-dependent T-lymphocyte proliferation, and infers that these cells contribute to the inferior prognosis following cryosurgery as compared to excision of a metastatic tumour.

Animals↗
PubMed1984

Absence of generalized immunosuppression in C57BL/6J mice implanted with Lewis T241 fibrosarcoma or Lewis lung carcinoma.

The immune status of C57BL/6J mice implanted with Lewis T241 fibrosarcoma or Lewis lung (LL) carcinoma was investigated on days 14 and 28 after implantation. Splenic lymphocyte responses were assessed in mitogen (Con A, LPS) mixed lymphocyte culture (MLC), natural killer (NK), graft-vs-host (GVH), and interleukin production assays. Except for NK-cell cytotoxicity, all other immunologic parameters were either comparable to those in medium-implanted controls or augmented. NK cytotoxicity was reduced in both tumor-bearing groups on day 28. The provision of NK potentiation therapy (beta-interferon, polyinosinic: polycytidylic acid) to T241 mice under various treatment conditions did not have any significant effect on lung metastasis or survival. The results of this study do not support the thesis that T241- or LL-bearing C57BL/6J mice are generally immunosuppressed. Indeed, when immune functions were assessed on the basis of total splenic activity, each of the measured immunologic parameters was substantially greater in animals with tumors than without. Further it seems improbable, considering the magnitude of the NK-cell defect in T241 mice on days 14 and 28 after implantation and the absence of a therapeutic response to NK-cell stimulants, that NK-cell cytotoxicity is intrinsically associated with resistance to tumor progression in this model.

Animals↗
PubMedDate not supplied

Palliative embolization of fibrosarcoma for control of tumor-induced hypoglycemia.

A 77-year-old woman with prior long-standing insulin-dependent diabetes presented with malignant hypoglycemia secondary to insulin-like substances excreted from a large unresectable fibrosarcoma of the left thigh. Partial embolization of the tumor supply from the deep femoral artery was performed using 150-250 microns polyvinyl alcohol foam particles. After embolization, the patient's serum glucose levels reverted to normal and she could be discharged from the hospital.

Aged↗
PubMed1987

DNA cross-linking following exposure to cis-platinum in primary and serially passaged cultured cells derived from two murine fibrosarcomas.

We compared the kinetics of the repair of total (ISC plus DPC) cross-links and of proteinase-resistant (ISC) cross-links in cultured cells derived from two murine fibrosarcoma tumors, FSA and NFSA, after treatment with cis-platinum (cis-DDP), using a modification of the alkaline elution technique. The two tumors had previously been characterized for their response to cis-DDP in vivo; FSA cells gradually removed cross-links from their genome, whereas the NFSA cells showed no capacity to repair these lesions. The aim of the present study was to establish whether treatment of cells from these same two tumors grown under controlled culture conditions would affect either the nature of the lesions induced by cis-DDP or the kinetics of repair of these lesions when compared with tumors treated with cis-DDP in vivo. The culture conditions represent two situations: in the first, the cells in culture approximated the proportion of tumor and normal host cells present in vivo, and in the second, the normal host cells had been eliminated by subculturing to produce cultures composed entirely of tumor cells. All cells were exposed to cis-DDP (either 10 or 20 micrograms/ml) for 1 h. The relative amounts of total cis-DDP-induced DNA crosslinks and of ISCs were then determined at various times after treatment. The results show that there was little difference in the behavior of these cultured cells compared to the in vivo response of the tumor from which they were derived. For FSA, each cell culture exhibited a capacity to repair DNA cross-links comparable to that of the tumor in vivo. For NFSA, the passaged cells again paralleled the behavior of that tumor in vivo, although in this case by showing no measurable capacity to repair cross-links. The absence of a significant repair response in the NFSA tumor therefore appears to be an intrinsic characteristic of these tumor cells.

Animals↗
PubMed1984

Expression of cell surface P-glycoprotein by an adriamycin-resistant murine fibrosarcoma.

Analysis of the cell membrane of Adriamycin (doxorubicin)-resistant UV-2237 ADMR murine fibrosarcoma cells revealed a 170,000-dalton component that is not found in the drug-sensitive parent or revertant cells. Immunoblot (Western blot) analysis showed that this component is similar to the 170,000-dalton P-glycoprotein found on the surface of Chinese hamster ovary cells that exhibit multidrug resistance. Thus, multidrug resistance and P-glycoprotein expression apparently can occur in a wide variety of cells, including the metastatic murine solid tumor cell line described here.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1979

Segregation of rat chromosomes in somatic cell hybrids between rat cells and HT 1080 human fibrosarcoma cells.

We produced somatic cell hybrids between HT 1080-6TG human fibrosarcoma cells and either rat white blood cells (WBC) or cells directly derived from rat spleen. Karyologic and isozyme analyses of hybrid cells indicated that they preferentially lose rat chromosomes. Hypoxanthine-aminopterine thymidine-selected hybrid clones expressing rat hypoxanthine phosphoribosyltransferase (HPRT), glucose-6-phosphate dehydrogenase (G6PD), and phosphoglycerate kinase (PGK) and containing the rat X chromosome were counterselected in a medium containing 30 micrograms/ml of 6-thioguanine. Concordant loss of the rat X chromosome and of the expression of rat HPRT and G6PD was observed in the hybrid clones.

Animals↗
PubMed1978

[Differentialdiagnostic problems in fibrosarcoma of the foot (author's transl)].

3 cases of fibrosarcoma of the foot are presented. Despite a history of pain up to several years the first radiological examination did not reveal any signs of a malignant tumor. X-rays taken 1/2 to one year later showed a localized osteolytic process. Then the diagnosis was established by biopsy. Consecutive x-rays and timing for a biopsy are discussed.

Bone Neoplasms↗
PubMed1983

Influence of vasoactive drugs on the intratumor distribution of blood flow and vascular volume in a transplantable rat fibrosarcoma.

The intratumor distribution of plasma volume and of blood flow was studied simultaneously by radioisotope techniques in a transplantable rat fibrosarcoma. Intravenous administration of norepinephrine changed the distribution of both plasma volume and blood flow to produce low values in tumor and in normal muscle. Intravenous administration of papaverine was surprisingly followed by similar effects, probably due to a direct influence of papaverine on cardiac function. Intraaortal administration of papaverine into the studied tissue area did not influence tumor blood flow or plasma volume but increased normal muscle plasma volume. The results might support a previously suggested possibility that one can directly influence the tumor vascular bed with vasoconstricting drugs, while tumor vessels are more resistant to pharmacologic dilatation probably because of their normal state of close to maximal dilatation.

Animals↗