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At least 973 records · Page 54Linked to original sources
PubMed1991

Platelet aggregation induced by adenosine diphosphate released from cloned murine fibrosarcoma cells is positively correlated with the experimental metastatic potential of the cells.

We established five clones (ML-01, ML-02, MH-01, MH-02, MH-03) from murine 3-methylcholanthrene-induced fibrosarcoma A (Meth A), and investigated their experimental metastatic potentials in relation to their platelet-aggregating activities. A clone with a high metastatic potential (MH-02) showed a characteristic biphasic pattern of platelet aggregation, of which the first peak was not present in the aggregation patterns of the clone with low metastatic potential (ML-01). The first peak was eliminated by treatment of the cells with apyrase, indicating that adenosine diphosphate (ADP) was the causative substance of this particular peak. The metastatic potential of clones correlated well with the ADP concentration of the culture media. These results suggest that the increased ADP production and consequential enhancement of platelet-aggregating activity are closely related to the increment of pulmonary metastatic potential of MH-02 clone.

Animals↗
PubMed1992

Somatic mutation during metastasis of a mouse fibrosarcoma line detected by DNA fingerprint analysis.

Metastatic nodules were examined by DNA fingerprint analysis. The probes used, Pc-1 and Pc-2, detect mutations as shifts in bands of the minisatellite loci which are dispersed among chromosomes. Four clonal lines of a fibrosarcoma from an F1 mouse (C57BL/Ka x C3H/He) were selected for various metastatic potentials upon inoculation into syngeneic mice. These four lines exhibited many extra bands resulting from recombination and/or DNA slippage, indicating accumulation of mutations during the successive passages in mice. One of the four, a 505 cell line which had been passaged extensively in vitro and consisted of a heterogenous population, was inoculated into thirteen syngeneic mice, and gave rise to six lung metastatic nodules in two mice. All the nodules showed band-patterns distinct from one another, although nodules within a given mouse tended to show similar patterns. When a genetically tagged 505-05-01 clone was analyzed, three of nine metastatic nodules obtained also revealed new bands. These results strongly suggest that somatic mutations occur at a high frequency during metastasis, providing direct evidence of genetic instability of the tumor cells.

Animals↗
PubMed1993

Progression of a weakly tumorigenic mouse fibrosarcoma at the site of early phase of inflammation caused by plastic plates.

To elucidate tumor progression-enhancing factor(s), we examined the effects of host inflammation and host immunological status on in vivo tumor progression. One x 10(4) cells of QR clones (QR-32, -20 and -18), regressor tumor clones of 3-methylcholanthrene-induced fibrosarcoma, were unable to grow when injected s.c. into C57BL/6 mice in cell suspension form. However, QR clones grew and were lethal when s.c. implanted, attached to plastic plates. Furthermore, the tumor lines (QRpP) obtained from the tumors which had arisen from the plate-attached QR-32 clone cells no longer required plastic plates for their growth in normal mice, and had acquired stable malignant phenotypes. Although QR-32 cells became lethal when injected at the site of plastic plate implantation 1, 5 and 10 days before tumor injection, few tumors developed when plastic plates had been implanted 20 or 30 days before tumor injection. We established culture clones from the tumors arising in normal mice and mice immunosuppressed by irradiation. Clones derived from the tumors which had arisen in normal mice after implantation with plastic plates were lethal when re-implanted in normal mice (71%). On the other hand, clones derived from the tumors that arose in irradiated mice with or without plastic plates were lethal in only a few normal mice, when re-implanted (20 and 8%, respectively). These results indicate that QR clone cell progression is enhanced by the early phase of inflammation at the site of plastic plate implantation and that the progression-enhancing activity of co-implantation with a plastic plate is inhibited by previous whole-body irradiation of hosts.

Animals↗
PubMed1994

Difference in allelic expression of genes probably associated with tumor progression in murine fibrosarcomas and cell lines.

Allelic expression was examined by single-strand conformation polymorphism analysis in murine fibrosarcomas from inter-subspecific F1 mice between C57BL/6 and MSM. Ten genes encoding p53, mdm2, E-cadherin, 72 kD metalloproteinase and its inhibitor (Timp2), thymidine kinase and four glucose transporters (Gluts) were examined. These genes were chosen because of their probable association with tumor development and progression. In some of the tumors and cell lines, p53, E-cadherin and Glut3 genes showed remarkable differences in allelic expression, one allele being poorly expressed. The allele-specificity persisted in nine cell lines obtained by repeated transplantations from one tumor. These results suggest that expression of some genes is allele-specific in tumor cells and the pattern of specificity is stable. Such a decrease or a loss of expression in one of the alleles may be functionally equivalent to the loss of heterozygosity of the gene, and therefore this may confer malignant properties on tumor cells. It is also suggested that differential expression of two alleles is a common event in tumor cells.

Alleles↗
PubMed1995

Isolation and properties of tumor-derived endothelial cells from rat KMT-17 fibrosarcoma.

Rat KMT-17 fibrosarcoma-derived endothelial cells were isolated by Percoll gradient centrifugation with an attaching-speed separation technique, and their properties in culture were examined. The primary cultured tumor-derived endothelial cells (TEC) showed angiotensin-converting enzyme activity, positivity for Factor VIII-related antigen staining, and typical capillary-like formation on Matrigel. The primary cultured TEC monolayer showed greater permeability than normal tissue-derived endothelial cell (aorta, vena cava and epididymal fat capillary) monolayers on FITC-dextran diffusion (molecular weight 70,000). Leukocyte adhesion to TEC was reduced compared to that to fat-derived capillary endothelial cells. These characteristics resembled those of tumor vascular endothelium, and were observed both in the primary and first-passage cell cultures, but not in the fourth-passage cell cultures. Our findings indicate that primary or subcultured TEC are applicable for studies of the physiological characteristics of tumor endothelial cells.

Animals↗
PubMed1996

Selective enhancement by tumor necrosis factor-alpha of vascular permeability of new blood vessels induced with agarose hydrogel-entrapped Meth-A fibrosarcoma cells.

We have previously developed a simple and quantitative method for assessment of in vivo tumor cell-induced angiogenesis by means of microencapsulation of tumor cells in agarose hydrogel and mouse hemoglobin ELISA (mHb-ELISA). In this article, we report that the new blood vessels induced with agarose-encapsulated tumor cells have the same sensitivity to tumor necrosis factor-alpha (TNF-alpha) as the original solid-tumor vessels. Agarose beads (average diameter = 200 microns), in which Meth-A fibrosarcoma cells were microencapsulated, were subcutaneously implanted in non-syngeneic ddY mice. Ten days later, extensive angiogenesis was observed on the implanted sites of Meth-A agarose heads, whereas no new blood vessels were induced with cell-free agarose heads. The vascular permeability of the new blood vessels induced with agarose-microencapsulated Meth-A cells was selectively and significantly enhanced by the i.v. injection of TNF-alpha, and it reached the maximum level at 2 h after the injection of TNF-alpha. At 4 h after the injection of TNF-alpha, the vascular permeability was reduced to the basal level. This permeability profile in Meth-A agarose beads in ddY mice is very similar to that in Meth-A solid tumor in syngeneic BALB/c mice. On the other hand, TNF-alpha-treatment did not affect the vascular permeability of other normal tissues or inflammatory tissue in ddY mice. These results strongly suggest that the new blood vessels induced with agarose-microencapsulated tumor cells have the specific characteristics of tumor vessels. Our in vivo angiogenesis assay system should be useful not only to screen anti-angiogenetic agents, but also to elucidate the mechanism of tumor angiogenesis.

Animals↗
PubMed1996

Inhibitory effect of a traditional Chinese medicine, Juzen-taiho-to, on progressive growth of weakly malignant clone cells derived from murine fibrosarcoma.

We have investigated the inhibitory effect of oral administration of Juzen-taiho-to, a Kampo (Chinese herbal) medicine, on progressive growth of a mouse fibrosarcoma. Spontaneously regressive QR-32 tumor cells were able to grow progressively in vivo when coimplanted s.c. with a foreign body, gelatin sponge, whereas QR-32 cells alone gradually grew for over 15 days after inoculation and thereafter regressed for up to 25 days. Oral administration of Juzen-taiho-to (40 mg/day/mouse) for 7 days after inoculation of QR-32 cells with gelatin sponge resulted in significant inhibition of tumor growth and prolongation of the survival of the tumor-bearing mice. This growth-inhibitory effect of Juzen-taiho-to observed on day 25 was dose-dependent over the dose range from 4 to 40 mg/day. Treatment with Juzen-taiho-to for 7 days before tumor inoculation with gelatin sponge also significantly suppressed tumor growth examined on day 25, as did the administration of bismuth subnitrate, which is well known to induce metallothionein, an antioxidant. On the other hand, inoculation of progressed tumor cells (QRsP) resulted in growth without gelatin sponge, leading to death in syngeneic mice. Administration of Juzen-taiho-to for 7 days after inoculation of QRsP cells resulted in a decrease of the tumor growth and prolongation of the survival of mice, but the effect was less than that on the growth of QR-32 regressor tumor after coimplantation with gelatin sponge. These results suggest that the inhibitory effect of Juzen-taiho-to is partly associated with prevention of gelatin sponge-elicited progressive growth, probably mediated by endogenous factors including antioxidant substances, in addition to the augmentation of host-mediated antitumor activity.

Administration, Oral↗
PubMed1999

Inhibition of experimental metastasis of human fibrosarcoma cells by anti-recombinant 37-kDa laminin binding protein antibody.

The laminin binding protein of 37 kDa (37LBP) is regarded as a precursor protein of the high-affinity 67-kDa laminin receptor (67LR). Expression of 67LR/37LBP is well correlated with biological aggressiveness of cancer, particularly with invasive and metastatic potential. To investigate in detail the role of 37LBP in cancer cells, we synthesized recombinant 37LBP (r37LBP) as a fusion protein and generated an IgG-type polyclonal antibody P4G against r37LBP. Western blot analysis with P4G showed a single band of 67LR under both nonreducing and reducing conditions using cell extract of human fibrosarcoma cells HT1080. It was shown that P4G inhibited cell attachment to immobilized laminin in a dose-dependent manner. Further, the intravenous injection of HT1080 cells pretreated with P4G, compared with that of cells pretreated with normal rabbit serum, resulted in a reduced number of experimental metastases (3.3+/-5.1 vs. 58.0+/-38.0 nodules per mouse, respectively) (P<0.005). These results suggest that P4G inhibits the colonization and growth of HT1080 cells in the lungs of mice, and that the blocking of r37LBP with the specific antibody P4G may offer a potential strategy for preventing cancer metastasis.

Amino Acid Sequence↗
PubMed2002

Expression of laminin-5 enhances tumorigenicity of human fibrosarcoma cells in nude mice.

Laminin-5 (LN5), which consists of laminin alpha3, beta3 and gamma2 chains, is a laminin isoform produced by various kinds of normal epithelial cells and tumor cells. Strong activity of LN5 in adhesion, migration and scattering of cells in vitro and its frequent detection in human tumor tissues have suggested a possible role of LN5 in the malignant growth of tumor cells. To examine whether LN5 affects the malignant potential of tumor cells, we prepared human fibrosarcoma HT1080 cell lines producing LN5 by transfecting a cDNA of laminin alpha3 chain into the parent cell line, which constitutively expressed the laminin beta3 and gamma2 chains. The exogenous alpha3 chain associated with the endogenous beta3 and gamma2 chains to secrete the LN5 heterotrimer that has strong cell-scattering and cell adhesion activities. The HT1080 transfectants expressing LN5 efficiently adhered to culture dishes in a serum-free condition as compared with control HT1080 cells, which secreted the monomers and heterodimer of the beta3 and gamma2 chains. When injected into nude mice subcutaneously, the HT1080 transfectants expressing LN5 grew faster and formed much larger tumors than the control cells. This suggests that LN5 promotes tumor growth in vivo.

Animals↗
PubMed1993

Procoagulant activity of the MC28 fibrosarcoma cell line in vitro and in vivo.

Experimental evidence suggests that many tumours can activate blood coagulation and that such interaction is part of the pathology of metastatic tumour growth. This study aimed to study the procoagulant activity of the methylcholanthrene-induced (MC28) fibrosarcoma to determine whether coagulation activation by these cells could explain the previously reported effects of oral anticoagulants on lung seeding in this model. MC28 cells shortened the recalcification times of normal and factor VII-deficient plasma and directly activated factor X in a chromogenic assay, but did not aggregate platelets in vitro in either whole blood or platelet-rich plasma. Cellular coagulant activity was calcium-dependent, blocked by DFP and concanavalin A but not inhibited by iodoacetamide, E-64 or antibodies to human tissue factor or factor VII. Injection of viable MC28 cells into hooded Lister rats induced a decrease in platelet count (P < 0.001), plasma factor X (P < 0.001) and fibrinogen (P < 0.05) and a marked increase in plasma haemoglobin (P < 0.001). These effects were either not observed or were considerably less marked in heparinized or warfarinized animals. Injection of MC28 cells treated with concanavalin A in vitro completely abolished the clotting changes observed with untreated cells. In conclusion, MC28 cells possessed a potent factor X-activating serine proteinase procoagulant in vitro, which had some of the characteristics of a tissue factor/factor VIIa complex. In vivo, MC28 cells caused clotting activation and intravascular fibrin generation. Since thrombocytopenia was abolished by heparin and the cells lacked platelet aggregating activity in vitro, thrombocytopenia was probably secondary to intravascular coagulation and thrombin generation. The trigger for intravascular clotting activation appeared to be the cellular procoagulant activity since it was abolished by prior in vitro blockade of the latter with concanavalin A.

Animals↗
PubMed1981

Density centrifugation of murine fibrosarcoma cells following in situ labelling with tritiated thymidine.

Murine fibrosarcoma (FSa) cells form at least five unique subpopulations after centrifugation in linear Renografin density gradients. Each of these subpopulations has been characterized with respect to selected kinetic parameters using pulse-labelling techniques and flow microfluorometry (FMF) analysis. Tumour-bearing mice were first injected intraperitoneally with a pulse label of tritiated thymidine ([3H]TdR, 50 microCi). Following 15, 30, 60 min or 24 hr these animals were injected with cold thymidine. Animals were killed, their tumours removed and made into suspension, and separated by density gradient centrifugation. Each gradient was fractionated and the density, cell number, tritium activity, and labelling index (LI) per fraction were determined. These data were then compared to FMF data for selected cell density, cell number, tritium activity, and labelling index (LI) per fraction were determined. These data were then compared to FMF data for selected cell density bands. The results indicated a relatively higher uptake of [3H]TdR in the cells recovered at the lighter (1.06-1.12 g/cm3) as compared to the heavier (greater than 1.12 g/cm3) densities. Following a 30-min pulse, the LI's of light cells (less than 1.12 g/cm3) ranged from 25 to 30%, while the heavier cells (greater than 1.12 g/cm3) had LI's between 10 and 15%. The unseparated control cells had an LI of 19%. comparable results were found at the other times tested. In contrast, the FMF profiles describing the DNA contents of the cells banding in the gradient showed no difference in proportion of S-phase cells among the separated subpopulations. This lack of correlation between the FMF determination of S-phase cells and labelling index for the denser cell populations implies that DNA content alone is not an effective measurement of the functional activity of cells in solid tumours. Finally, the relatively reduced uptake of [3H]TdR by these denser cells suggests that they may have resided at relatively large distances from the functional vasculature in the tumour.

Animals↗
PubMed2006

Calcium salicylate-mediated apoptosis in human HT-1080 fibrosarcoma cells.

Salicylates are novel biologically active compounds that exhibit multiple therapeutic activities. The anti-cancer effectiveness of calcium salicylate has been investigated on human HT-1080 fibrosarcoma cell lines at relatively low concentrations (predominantly 0.4 mM) compared to those previously reported. Although low calcium salicylate concentrations did not retard tumour growth progression significantly, as measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and time-lapse assays, its cytotoxic characteristics were proven to be prominent by various morphological and immunocytological techniques. The results here demonstrate evidence for approximately 25% apoptosis after treatment with calcium salicylate, which up-regulatd the expression of p53, p21 and Bax, and down-regulated Bcl-2 in HT-1080 cells.

Antineoplastic Agents↗
PubMed1991

Piroxicam, indomethacin and aspirin action on a murine fibrosarcoma. Effects on tumour-associated and peritoneal macrophages.

Growth of a methylcholanthrene-induced fibrosarcoma in BALB/c mice was accompanied by an increase in the activation state of tumour-associated macrophages (TAM), as measured by their FcIgG receptor expression, phagocytic index and beta-glucuronidase levels. All of these parameters were markedly higher in TAM than in peritoneal macrophages (PM) derived from the same animal. On the other hand, PM from tumour-bearing mice showed lower activation parameters than PM from normal animals. We also studied the effect on tumour development of three inhibitors of prostaglandin synthesis: indomethacin, piroxicam and aspirin. Intraperitoneal administration of these drugs during 8 d was followed by the regression of palpable tumours. Indomethacin (90 mg/d) induced 45% regression, while with piroxicam (two 400 mg/d doses and six 200 mg/d doses) and aspirin (1 mg/d) 32% and 30% regressions, respectively, were observed. The growth rate of nonregressing tumours, which had reached different volumes by the end of the treatment, was delayed to a similar extent by the three anti-inflammatory non-steroidal drugs (NSAID). With respect to TAM, the treatment did not induce any significant change in their activation state, though both piroxicam and indomethacin increased slightly the TAM number. In contrast, NSAID administration was followed by a remarkable increase in the activation parameters of PM when compared with PM from tumour-bearing mice receiving no treatment. Indeed, these parameters were in some cases higher than those of PM from normal mice. The leukocytosis (60,000/microliters) with neutrophilia (80%) induced by tumour growth on peripheral blood leukocytes (PBL) was reversed by the treatment to values close to normal, in parallel with the reduction of tumour size. A drop in haematocrit was also noted which was most probably a consequence of tumour growth rather than of the treatment. This study reveals that the three NSAID tested have a remarkable antitumour activity, which correlates with the restoration of PM activity and PBL values.

Animals↗
PubMed1975

Hypoglycaemia associated with an intrathoracic fibrosarcoma.

A patient with an intrathoracic fibrosarcoma in whom disabling hypoglycaemic episodes occurred is reported. No further hypoglycaemic episodes occurred following removal of the tumour. The mechanism of the hypoglycaemia associated with non-pancreatic tumours is discussed. It seems that inadequate hepatic glucose output was an important factor in contributing to the hypoglycaemia in this patient.

Aged↗
PubMed1995

Radiation-induced fibrosarcoma of the tongue.

Three patients with a radiation-induced fibrosarcoma of the tongue are presented. All three patients had interstitial radiotherapy and tumour-induction by irradiation seems to be the most likely explanation for the tumour in these patients.

Aged↗
PubMedDate not supplied

Fibrosarcoma arising in a lumbosacral meningocoele.

A 53 year old woman presented with enlargement of a sacral meningocoele and pain in the back and legs. She died from a pulmonary embolus. Fibrosarcoma, apparently arising in the sacral region, involved the leptomeninges and nerve roots as far rostrally as the pons. Nine previously reported cases are discussed.

Female↗
PubMed1991

Near triploidy in a feline fibrosarcoma.

A seven-year-old male cat developed a subcutaneous fibrosarcoma. The numerical cytogenetic evaluation of the tumour revealed the presence of 69.2% of cells in the near-triploid chromosome range between 51 and 64. The copy numbers of the different chromosomes were widely distributed from monosomies up to heptasomies. Two giant chromosomes were regularly present.

Animals↗