Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “FIBROSARCOMA”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 703 records · Page 39Linked to original sources
PubMed1994

A novel in vitro assay system for transendothelial tumor cell invasion: significance of E-selectin and alpha 3 integrin in the transendothelial invasion by HT1080 fibrosarcoma cells.

The interaction of tumor cells with endothelial cells is a key event in tumor metastasis. We established an in vitro invasion assay system, in which the invasion of tumor cells after interaction with endothelial cells can be examined. Two chamber culture wells separated by porous membrane were used. Human umbilical vein endothelial cells (HUVEC) were placed on porous membranes coated with matrix components. The invasion by HT1080 fibrosarcoma cells was determined in this system by counting the number of cells that moved through the membranes from upper to lower chambers. HUVEC cells did not migrate through the membranes as judged by the staining with UEA-I. Observation by scanning electron microscopy revealed that HT1080 cells bound to HUVEC surfaces and migrated underneath the HUVEC monolayer. Effects of antibodies specific for cell surface adhesion molecules on the migration of HT1080 cells were examined. Invasion of uncoated membranes and membranes coated with HUVEC cells was compared. Antibody against E-selectin significantly suppressed an increase of HT1080 cell invasion of HUVEC monolayers stimulated by IL-1 beta or TNF alpha. Antibody against integrin alpha 3 subunit remarkably inhibited the invasion of HUVEC cell-coated membranes, suggesting that integrins with the alpha 3 subunit may play an important role in the transendothelial invasion by HT1080 cells.

Cell Adhesion Molecules↗
PubMed1994

Differential purification of autocrine motility factor derived from a murine protein-free fibrosarcoma.

We have previously shown that a protein-independent growing fibrosarcoma, Gc-4 PF has a high motile response to its cultured medium, which is associated with an increase in expression of gp78, a cell surface receptor for autocrine motility factor (AMF). Here we show that the cultured medium contains two motile activities, acidic and basic AMFs with regard to binding features on ion exchange chromatography. These two AMFs were purified by sequential DEAE anion exchange, CM cation exchange, and gel filtration chromatographies. However, both acidic and basic AMFs have a similar size of 55 kDa and 65 kDa under non-reducing and reducing conditions, respectively, with the same pI of 6.5. The stimulated motility of both AMFs was inhibited by the pertussis toxin (PT), but not by Streptomyces hyaluronidase. These two AMFs significantly stimulated the lung colonizing properties of the self-producing cells by 1.5-fold. These results suggest that both acidic and basic AMFs may correspond to the previously reported AMF and confirm directly that the AMF-gp78 signaling pathway is involved in cell motility associated with metastatic property.

Animals↗
PubMedDate not supplied

Dynamic heterogeneity: experimental metastasis studies with RIF-1 fibrosarcoma.

We have examined the metastatic behaviour of cells from a series of clones of RIF-1 fibrosarcoma, a recently derived murine tumour. The clones were grown to different sizes (small: 10(5)-10(6) cells and large approximately 2 x 10(7) cells) and their metastatic potential was quantified using an experimental metastasis assay. There was significant variability between the metastatic potential of clones derived from the same population. Furthermore large clones had higher metastatic efficiency (metastases/cell injected) than the small clones derived from the same population. The results from these experiments indicate that metastatic variants are generated during the growth of the clones. The mean effective rate of generation of metastatic variants was estimated using Luria-Delbruck fluctuation analysis to be 1.7 x 10(-5)/cell/generation. The data described are consistent with a dynamic heterogeneity model of metastasis, in which the variant phenotypes are postulated to arise in growing tumour cell populations at a high rate but need not be stable in order to produce metastases. The results thus indicate that the model is applicable to a recently derived tumour as well as the extensively transplanted KHT sarcoma, B16 melanoma and OTF9 embryonal cell carcinoma.

Animals↗
PubMed1992

Comparative effects of a recombinant and a mutein type of granulocyte colony stimulating factor on the growth of Meth-A fibrosarcoma with 5-fluorouracil chemotherapy.

The present study was designed to evaluate the effects of a recombinant human G-CSF (rhG-CSF) and a mutein G-CSF (KW-2228) on leucopenia and tumor growth in mice treated with 5-fluorouracil (5-FU). In normal mice, the number of leucocytes (white blood cell, WBC) reached the peak 12 hours after a single injection of either type of G-CSF and decreased to the normal level after 24 hours. Daily administration induced a continuous increase in the WBC count, however, administrations at intervals did not. Meth-A fibrosarcoma was subcutaneously inoculated into the backs of syngeneic BALB/c mice. The mice were treated with 5-FU alone or with G-CSFs. Chemotherapy with 5-FU alone resulted in leucopenia and an insignificant inhibition of tumor growth. The conjunctive administration of G-CSFs with 5-FU resulted in a significantly augmented inhibition of tumour growth, and leukopenia was not seen. This augmenting effect was more prominent with KW-2228. These results suggest that in 5-FU chemotherapy G-CSFs may be beneficial in restoring the number of leucocytes from leucopenic state and in augmenting the tumor inhibitory effect. Furthermore, KW-2228 may be more beneficial than the natural type rhG-CSF.

Amino Acid Sequence↗
PubMed1990

The effect of radiation therapy combined with natural killer cells against spontaneous murine fibrosarcoma.

The effect of radiation therapy combined with lymphoid cells against spontaneous murine fibrosarcoma (FSa-II) was investigated both in vivo and in vitro. In the in vivo experiment, syngeneic C3H mice were divided into 3 groups. Animals in the first group were injected with 1 x 10(5) tumor cells into the right hind leg. Animals in the second and third groups were injected with 1 x 10(5) tumor cells mixed with 1 x 10(7) normal lymphoid cells (NLC) or effector lymphoid cells (ELC), respectively. ELC were obtained from spleen and lymph nodes of FSa-II-bearing mice and incubated in vitro for 40 hr to eliminate suppressor T cell function. NLC were obtained from normal mice and incubated in the same way. Irradiation was given using 137Cs unit 3 days after cell inoculation. 12 out of 14 mice (85.7%) inoculated with tumor cells mixed with NLC did not show any tumor growth at 60 Gy local irradiation. 12 out of 21 mice (57.1%) inoculated with tumor cells alone and 6 out of 10 (60%) with tumor cells mixed with ELC rejected tumors at the same radiation dose. This synergistic effect with NLC was not observed when NLC was inoculated after irradiation, indicating that lymphoid cells should be in contact with tumor cells before irradiation. In the 51Cr release assay, lymphoid cells obtained from whole body irradiated (WBI) mice showed 17.8% lysis without irradiation and 28.8% lysis at 5 Gy irradiation. Untreated NLC showed almost no cytotoxic effect at the same radiation dose. This synergistic effect disappeared when WBI lymphoid cells were treated with anti asialo GM1 and complement.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Infantile fibrosarcoma: radiological and clinical features.

Two cases of infantile fibrosarcoma are described. This rare childhood malignancy of mesodermal origin usually affects the lower limbs, as it did in both of our cases. Previously, the only treatment option available involved some form of radical and often mutilating surgery. More recently, combination chemotherapy has given good results, with the effect that various imaging modalities have become important in assessing both the initial extent of disease and the response to treatment. Computed tomography has the advantage of demonstrating the amount of osseous involvement, but at the expense of a considerable dose of ionizing radiation. On the other hand, magnetic resonance imaging, with its multiplanar capacity, gives superior demonstration of breaching of tissue planes, which has important implications for planning of surgery. However, as in other soft tissue tumours, changes in signal characteristics with treatment have proved less specific than was originally anticipated.

Bone Resorption↗
PubMed1992

Effects of n-3 and n-6 fatty acids on tumor necrosis factor cytotoxicity in WEHI fibrosarcoma cells.

Modulation by fatty acids of the cytotoxic effect of recombinant tumor necrosis factor alpha (TNF) toward WEHI 164 mouse fibrosarcoma cells has been examined. Preincubating the highly TNF-sensitive WEHI clone 13 cells for 44 hr with 50 mumol/L of 20:5n-3, 22:6n-3, 18:3n-6, 20:3n-6 or 20:4n-6 reduced cell survival 22 hr after challenge with TNF (40 ng/L) by 65%, 72%, 60%, 98% and 85%, respectively. In comparison, 18:3n-3, 18:2n-6 and 18:1n-9 had only negligible effects on TNF-induced toxicity. Different extent of fatty acid incorporation into cell total phospholipids or triglycerides could not explain the observed effects on TNF cytotoxicity, and the enhanced cytotoxicity could therefore not be explained merely by an increased unsaturation of the cell membranes. In addition to the fatty acid supplied, preincubation with 18:2n-6, 18:3n-6 or 18:3n-3 also enriched the cells with 20:2n-6, 20:3n-6 and 20:3n-3, respectively, most likely due to chain elongation. The results suggest that the WEHI cells have a low delta 6 desaturase activity, and that n-6 and n-3 acids must have at least 3 or 4 double bonds, respectively, to enhance TNF cytotoxicity in WEHI cells. Dexamethasone partly inhibited TNF-induced cytotoxicity, while cyclooxygenase, thromboxane synthetase or lipoxygenase inhibitors had no or negligible effects. The antioxidant butylated hydroxyanisole (BHA) completely inhibited TNF-induced cytotoxicity, while the structurally and functionally similar antioxidant butylated hydroxytoluene had no such effect, indicating that BHA does not block TNF cytotoxicity through its antioxidant effect.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Basic fibroblast growth factor, albumin, and transferrin purified from rat rhodamine fibrosarcoma tissue are all essential for growth of primary tumor cells from the same tissue in serum-free medium.

Primary Rhodamine fibrosarcoma (RdF) cells from rats were shown to grow in serum-free medium supplemented with basic fibroblast growth factor (bFGF), albumin, and transferrin, all of which were purified from RdF tissue. Their growth rate with these supplements was similar to that of cells in medium supplemented with calf serum. bFGF purified from RdF tissue (Rd-bFGF), which was previously designated as DNA synthesis factor, stimulated the growth of primary RdF cells maximally at 30 ng/ml in the presence of the other two proteins. Albumin and transferrin were separated from partially purified tumor growth stimulating activity which was previously shown to stimulate growth of primary RdF cells in serum-free medium. The albumin (RdA) and transferrin (RdT) found in the extract of RdF tissue were not due simply to contamination of the tissue with blood, but to their accumulations in the tissue. The growth stimulatory activities of RdA and RdT on primary RdF cells in serum-free medium were maximal at 30 and 10 micrograms/ml, respectively. These results suggest that Rd-bFGF, RdA, and RdT, all of which accumulate in the tumor tissue, are essential for growth of RdF cells in the tissue.

Albumins↗
PubMed1990

A case report of primary fibrosarcoma of the liver.

A 75-year-old woman was admitted to our hospital complaining of right hypochondrial pain. Echo sonography and computed tomography demonstrated a large tumor with irregular internal density in the right lobe of the liver. Angiography revealed a moderately hypervascular tumor. She was treated with transcatheter arterial embolization. Three weeks later, the tumor ruptured. She died of accompanying acute myocardial infarction seven months after the onset of the illness. Autopsy revealed primary fibrosarcoma of the liver. The tumor appearance varied from firm whitish to soft myxomatous. A part of the tumor showed hemorrhagic necrosis. There was no intrahepatic metastasis. The tumor tissue was composed of spindle shaped cells and immunohistochemically stained with vimentin.

Aged↗
PubMed1980

Buoyant density of EMT6 fibrosarcoma cells: time course of the density changes after growth in hypoxia.

EMT6 fibrosarcoma cells were grown to the exponential phase in tissue culture and incubated at 37 degrees C under hypoxic conditions. Buoyant density was determined as a function of the time in hypoxia. Hypoxia was produced in two ways. The first involved incubation of the cells in sealed aluminum chambers containing 95% N2, 5% CO2 gas, and < 10 ppm oxygen, resulting in the cells rapidly becoming exposed to the hypoxic environment. After incubation at 37 degrees C, they were centrifuged in linear Ficoll gradients to their isopycnic density. A significant decrease in density was found after 4 h, and prolonged incubation up to 24 h did not result in further change. This density change was reversible on transfer back to aerobic conditions, with the hypoxic cells reverting to their aerobic density after about 10 h reincubation in air. The second method of producing hypoxia involved growing about 8 X 10(6) cells in a medium-filled air-tight container. Hypoxia was produced gradually as the oxygen in the medium was consumed by cellular respiration. Similar results were obtained; that is, hypoxic cells became significantly less dense. However, when the level of hypoxia was varied between 4000 and < 10 ppm at 2-h intervals after the cells had depleted all of the original oxygen, no significant difference in density was found between hypoxic and aerobic cells.

Animals↗
PubMedDate not supplied

Hyaluronidase induces murine L929 fibrosarcoma cells resistant to tumor necrosis factor and Fas cytotoxicity in the presence of actinomycin D.

Actinomycin D (ActD) enhances the potency of tumor necrosis factor-alpha (TNF-alpha) in killing cancer cells. However, it is determined in this study that murine L929 fibrosarcoma cells, when pretreated with bovine testicular hyaluronidase for 12-24 h, became resistant to the cytotoxic effect of TNF-alpha in the presence of DNA intercalators, such as ActD, doxorubicin, and daunorubicin. Monoclonal anti-Fas antibody-mediated apoptosis in the presence of ActD was also blocked in hyaluronidase-pretreated L929 cells. Hyaluronidase failed to up- or downregulate the expression of apoptosis regulatory proteins, including Bcl-2, Bcl-xL, ICH-1, and TIAR, suggesting that these proteins were not involved in the hyaluronidase-induced resistance to TNF/ActD. A semisynthetic polysulfated hyaluronic acid (HA) inhibited the increased TNF/ActD resistance, whereas unmodified HA, dextran sulfate, and naturally polysulfated glycosaminoglycans had no effect. Evidence is provided here that the induced resistance is related to serum fetuin and a novel intracellular 35-kDa TNF-binding protein (intra TBP). Under serum-free conditions, L929 became refractory to TNF/ActD cytotoxicity and hyaluronidase reversed the resistance. Exogenous fetuin increased L929 cell spreading and proliferation, and restored hyaluronidase-induction of TNF/ActD resistance in these serum-starved cells. Hyaluronidase failed to reduce the expression of TNF-receptors and their binding of TNF-alpha. However, binding and Western-blotting analyses revealed that hyaluronidase downregulated the intra-TBP. Overall, these observations suggest that serum fetuin and intraTBP are involved in the hyaluronidase induction of TNF/ ActD resistance.

Animals↗
PubMed1993

Phenotypical and functional analyses of mononuclear cells during rejection of a transplanted murine fibrosarcoma.

Repeated injections of mitomycin C-treated T2 fibrosarcoma cells into tumor-sensitized mice cause regression of a secondary tumor graft and more than 90% of the mice are cured. In the data presented here, an enhancement of the cytolytic cell-mediated activities measured in vitro against the specific T2 targets is shown in lymph nodes draining the tumor and in the spleen during the process of tumor rejection. Histopathologic studies revealed a rapid and marked accumulation of mononuclear cells mostly at the periphery of the rejected tumor tissue. A significant increase of CD8-positive, asialo GM1-positive and acid phosphatase-positive cells was observed in the rejected tumors whereas CD4-positive cells were similarly detected in both progressing and rejected tumor tissue. As macrophages seemed to be the population presenting the most persistent variation after immunization, the production of TNF-alpha was studied within the tumor site and in the lymphoid tissues during the regression process. Firstly, the presence of TNF-alpha within the cytoplasm of most of the adherent cell fractions isolated from the spleen and the tumor of immune mice was demonstrated by immunocytochemistry. Next, TNF-alpha mRNA-containing cells were determined by in situ hybridization of frozen tumor sections and identified essentially as tumor infiltrating macrophages. Finally, the macrophage populations isolated from tumors and from the spleen of immune mice were able to produce in vitro large quantities of TNF-alpha without exogenous stimulation. These findings support the role of TNF-alpha in the effector mechanisms contributing to the tumor regression process.

Animals↗
PubMed2005

Distinct different intra-tumor distribution of FDG between early phase and late phase in mouse fibrosarcoma.

An early image of intra-tumor distribution of 14C-labeled fluorodeoxy glucose (14C-FDG) was compared with a late image of 18F-labeled FDG (18F-FDG) using mouse fibrosarcoma. Heterogeneous intra-tumor distribution of 14C-FDG was observed 1 minute post injection of the tracer, whereas relatively homogeneous distribution of 18F-FDG was seen 30 minutes later. 14C-FDG was particularly taken up in the peripheral part of the tumor immediately after the tracer injection. A gradual and significant increase in 18F-FDG accumulation with time was seen in the central part of tumor, which indicated an enhancement of anaerobic glycolysis. An initial uptake of 18F-FDG was also compared with distribution of 14C-iodoantipyrine and 14C-thymidine uptake. Intratumoral distribution of initial uptake of 18F-FDG showed almost the same regional distribution of 14C-iodoantipyrine. A similar distribution of 14C-thymidine as the initial uptake of 18F-FDG was also observed. These results indicated that a high initial FDG uptake area seemed to be highly proliferative. A significant difference in the intratumoral distribution of FDG between early phase and late phase seemed to be related to heterogeneous biological characteristics of tumor cells.

Animals↗
PubMedDate not supplied

Malignant fibrosarcoma with features of myxoma.

Left atrial tumor, diagnosed as myxoma at first investigation, was later demonstrated to be a malignant fibrosarcoma with myxoid change. Myxoma should be diagnosed and managed carefully because of its wide range of histopathologic features.

Adolescent↗
PubMed2001

Fibrosarcoma in bizarre parosteal osteochondromatous proliferation.

Bizarre parosteal osteochondromatous proliferation (BPOP) is a rare benign lesion predominantly involving the small bones of the hands and feet. Malignant transformation in BPOP has not been documented in the English literature. This report presents the coexistence of fibrosarcoma with BPOP in the right distal fibula of an 18-year-old woman.

Adolescent↗
PubMed1997

Sclerosing epithelioid fibrosarcoma: short T2 on MR imaging.

A case of sclerosing epithelioid fibrosarcoma and its appearance on MRI is presented. The tumor showed a zonal architecture on MRI with a large central core of very low signal intensity and a peripheral rim of intermediate to high signal intensity on T1- and T2-weighted spin echo pulse sequences. The core showed decreased cellularity with dense collagen deposition on histologic examination, and the peripheral zone increased cellularity with increased nuclear atypia. The presence of a prominent region of very low signal intensity on T1- and T2- weighted images can be seen with neural tumors, giant cell tumor of the tendon sheath, aggressive fibromatosis, and, in rare instances, with soft tissue sarcomas rich in collagen.

Adult↗
PubMed2006

CD40 ligation restores cytolytic T lymphocyte response and eliminates fibrosarcoma in the peritoneum of mice lacking CD4+ T cells.

Absence of CD4(+) T cell help has been suggested as a mechanism for failed anti-tumor cytotoxic T lymphocytes (CTL) response. We examined the requirement for CD4(+) T cells to eliminate an immunogenic murine fibrosarcoma (6132A) inoculated into the peritoneal cavity. Immunocompetent C3H mice eliminated both single and repeat intraperitoneal (IP) inoculums, and developed high frequency of 6132A-specific interferon-gamma (IFNgamma)-producing CTL in the peritoneal cavity. Adoptive transfer of peritoneal exudate cells (PEC) isolated from control mice, protected SCID mice from challenge with 6132A. In contrast, CD4 depleted mice had diminished ability to eliminate tumor and succumbed to repeat IP challenges. Mice depleted of CD4(+) T cells lacked tumor-specific IFNgamma producing CTL in the peritoneal cavity. Adoptive transfer of PEC from CD4 depleted mice failed to protect SCID mice from 6132A. However, splenocytes isolated from same CD4 depleted mice prevented tumor growth in SCID mice, suggesting that 6132A-specific CTL response was generated, but was not sustained in the peritoneum. Treating CD4 depleted mice with agonist anti-CD40 antibody, starting on days 3 or 8 after initiating tumor challenge, led to persistence of 6132A-specific IFNgamma producing CTL in the peritoneum, and eliminated 6132A tumor. The findings suggest that CTL can be activated in the absence of CD4(+) T cells, but CD4(+) T cells are required for a persistent CTL response at the tumor site. Exogenous stimulation through CD40 can restore tumor-specific CTL activity to the peritoneum and promote tumor clearance in the absence of CD4(+) T cells.

Adoptive Transfer↗
PubMed2006

N-acetylneuraminic acid coupled human recombinant TNFalpha exhibits enhanced anti-tumor activity against Meth-A fibrosarcoma and reduced toxicity.

In order to study the effect of glycosylation on its biological activities and to develop tumor necrosis factor alpha (TNFalpha) with less deleterious effects, N-acetylneuraminic acid (NeuAc) with a C9 spacer was chemically coupled to human recombinant TNFalpha. NeuAc-coupled TNFalpha (NeuAc-TNFalpha) exhibited reduced activities in vitro by about threefold compared to native TNFalpha. In this study, we examined a variety of TNFalpha activities in vivo. NeuAc-TNFalpha reduced activities in the up-regulation of serum levels of IL-6 and NOx, but comparable activity as native TNFalpha in the down-regulation of the serum level of glucose. However, NeuAc-TNFalpha was more potent than TNFalpha in the up-regulation of the serum level of serum amyloid A (SAA). NeuAc-TNFalpha was less toxic to mice. In addition, NeuAc-TNFalpha exhibited an augmented anti-tumor activity against Meth-A fibrosarcoma without hemorrhagic necrosis. These results indicate that coupling with NeuAc enabled us to develop neoglycoTNFalpha with selective activities in vivo, including enhanced anti-tumor activity but reduced toxicity.

Animals↗