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PubMed2001

Evidence of nerve sheath differentiation and high grade morphology in sclerosing epithelioid fibrosarcoma.

Sclerosing epithelioid fibrosarcoma is a recently described sarcoma in which ultrastructural evidence of fibroblastic differentiation forms part of the diagnostic criteria. This report describes a further case of this tumour, which showed evidence of both fibroblastic and perineurial differentiation by immunohistochemistry and electron microscopy, and which had areas of high grade morphology. The tumour metastasised and the patient died of disease 12 months after presentation. The relevance of these findings to diagnosis and differentiation in these tumours is discussed.

Cell Differentiation↗
PubMed1991

Molecular species of phospholipid in rats in primary and transplanted fibrosarcomas induced by soybean oil containing tocopherol acetate.

When soybean oil containing tocopherol acetate was given to rats once a week subcutaneously for 10-12 months, it caused the development of fibrosarcomas at the injection site in 11 of 15 rats. A tumor produced in this manner proved eminently transplantable into other rats. The molecular species of phospholipid subclasses were determined in primary and transplanted tumors. The molecular species composition of the phospholipid subclasses in both types of tumors were similar. The percentages of diacyl and alkylacyl glycerophosphocholine (GPC) were 90-93 and 6-8% of total phosphatidylcholine, respectively. The percentages of diacyl and alkenylacyl glycerophosphoethanolamine (GPE) were 51 and 45%, respectively, of total phosphatidylethanolamine (PE). Diacyl and alkylacyl GPC species containing arachidonic acid (20:4) composed about 15-16 and 37-40% of each subclass, respectively. Diacyl and alkenylacyl GPE species containing 20:4 composed about 38-40 and 56-60% of each subclass, respectively. Disaturated species of diacyl and alkylacyl GPC composed about 22-24 and 13% of each subclass, respectively, whereas these species of PE composed less than 2%. The fatty acid composition of the other tumor phospholipids was analyzed.

Animals↗
PubMed2003

Anti-metastatic effects of fuzhengfangaitang on human fibrosarcoma cells HT1080.

Fuzhengfangaitang (FZFAT) is used to inhibit recurrence and metastasis of cancer in the clinic. By applying an in vitro invasion assay model, we examined the antimetastatic effect of FZFAT. In the 3H-thymidine incorporation assay, FZFAT-treated groups showed a decreased DNA synthesis rate compared with the control group (F-value 87.42981, P-value 2.02E-08, F0.05(3,12) 3.4903). Gelatin zymogram assay showed that FZFAT decreased the gelatinolytic activity of matrix metalloproteinases-9 (MMP-9) from human fibrosarcoma cell line (HT-1080), at concentrations of 200 and 400 microg/ml. In the MMPs dot blotting assay, FZFAT inhibited the expression of MMP-1 at concentration of 100 microg/ml, and MMP-9 at concentrations of 200 and 400 microg/ml. Western blots for AP-1 and its signal mediators Erk and JNK showed that expression of Fos and JNK were decreased by the addition of FZFAT at 300 microg/ml, whereas Erk was not. Therefore it was evident that FZFAT regulated the expression of MMP-9 through its transcription factor AP-1 and the signal mediator JNK. We examined whether FZFAT inhibited the invasion of HT-1080 cells through matrigel precoated transwell chambers. The results showed that FZFAT effectively inhibited the invasion of HT-1080 cells as compared with the control phorbol 12-myristate-13-acetate (+PMA) groups (t-value 5.871584, P-value 0.013901, t0.05(2) 2.919987). From our research, part of the mechanism underlying the antimetastatic effect of FZFAT has been elucidated in vitro.

Antineoplastic Agents, Phytogenic↗
PubMed1975

An assessment of RBE of Californium-252 for C57-Black/6 mouse fibrosarcoma by a precise afterloading technique.

Afterloading techniques were developed for the in vivo assessment of the RBE of californium-252 with respect of radium-226 using a fibrosarcoma in mice. The afterloading holder positions sources so that the tumor is uniformly irradiated. Using the end points of tumor volumetric studies up to 150 days after irradiation, it was found that the RBE ranged from 5-8 at clinically relevant dose rates and total doses.

Animals↗
PubMed1977

Combined radiotherapy and Corynebacterium parvum treatment of a murine fibrosarcoma.

A single dose of Corynebacterium parvum (Cp) at 70 microgram, 175 microgram or 350 microgram was effective in suppressing the growth of a subcutaneous fibrosarcoma and occasionally in inducing complete regression and in prolonging the survival time of C3H/HeJ tumor-bearing mice. A single exposure of x rays at 2,000 rads induced some complete regression, but a higher number of complete regressions was induced by combined x-ray and Cp treatment. In the combined x-ray and Cp treatment, Cp given on the same day immediately after x irradiation was best. When 70 microgram of Cp was given a few days before x rays, the intravenous and intraperitoneal routes were better than the intratumor route of injection.

Animals↗
PubMed1978

Multiple adjuvant therapy on a murine fibrosarcoma: actinomycin-D, X-irradiation and local tumor hyperthermia.

The tumoricidal activities of single dose x-irradiation (RAD) and concomitant Actinomycin D (AMD) with or without local tumor hyperthermia (LTH) on an in vivo Methylcholanthreme-induced fibrosarcoma (Meth-A) are described. The addition of LTH enhanced the actions of AMD, RAD and AMD + RAD; the trimodality treatment was most effective. Based on delay of tumor growth, the radiation dose reduction factors for AMD + RAD + LTH compared to RAD; AMD + RAD + LTH, were approximately 2.8, 2.1, and 1.8, respectively. The shape of the curves suggests a further decrease in the ability of the tumor cell to repair sublethal damage with AMD + RAD + LTH. The clinical relevance is not determined.

Animals↗
PubMed1983

Nuclear magnetic resonance imaging of a fibrosarcoma tumor implanted in the rat.

Fibrosarcoma tumor cells were implanted in the hind legs of 25 rats and studied from the first to the sixth week postimplantation. Nuclear magnetic resonance imaging detected all tumors and did not yield any false-positives in five control rats. The T1 relaxation values of tumors overlapped those of muscle, and the T2 values overlapped those of fat, but the combination of the two values allowed discrimination of each of the three tissues with no overlap. The difference in relaxation time between tumor and muscle could be accounted for on the basis of water content, which was approximately 14% higher in the tumors. This study confirms data from previous studies suggesting that nuclear magnetic resonance imaging is a highly sensitive modality, but that T1 and T2 values are not specific for individual pathologic conditions.

Adipose Tissue↗
PubMed2005

Early detection of tumor response to chemotherapy by 3'-deoxy-3'-[18F]fluorothymidine positron emission tomography: the effect of cisplatin on a fibrosarcoma tumor model in vivo.

We have assessed the potential of [18F]fluorothymidine positron emission tomography ([18F]FLT-PET) to measure early cytostasis and cytotoxicity induced by cisplatin treatment of radiation-induced fibrosarcoma 1 (RIF-1) tumor-bearing mice. Cisplatin-mediated arrest of tumor cell growth and induction of tumor shrinkage at 24 and 48 hours, respectively, were detectable by [18F]FLT-PET. At 24 and 48 hours, the normalized uptake at 60 minutes (tumor/liver radioactivity ratio at 60 minutes after radiotracer injection; NUV60) for [18F]FLT was 0.76 +/- 0.08 (P = 0.03) and 0.51 +/- 0.08 (P = 0.03), respectively, compared with controls (1.02 +/- 0.12). The decrease in [18F]FLT uptake at 24 hours was associated with a decrease in cell proliferation assessed immunohistochemically (a decrease in proliferating cell nuclear antigen labeling index, LI(PCNA), from 14.0 +/- 2.0% to 6.2 +/- 1.0%; P = 0.001), despite the lack of a change in tumor size. There were G1-S and G2-M phase arrests after cisplatin treatment, as determined by cell cycle analysis. For the quantitative measurement of tumor cell proliferation, [18F]FLT-PET was found to be superior to [18F]fluorodeoxyglucose-PET (NUV60 versus LIPCNA: r = 0.89, P = 0.001 and r = 0.55, P = 0.06, respectively). At the biochemical level, we found that the changes in [18F]FLT and [18F]fluorodeoxyglucose uptake were due to changes in levels of thymidine kinase 1 protein, hexokinase, and ATP. This work supports the further development of [18F]FLT-PET as a generic pharmacodynamic readout for early quantitative imaging of drug-induced changes in cell proliferation in vivo.

Adenosine Triphosphate↗
PubMed2005

Reduction of experimental human fibrosarcoma lung metastasis in mice by adenovirus-mediated cystatin C overexpression in the host.

Tumor cell invasion and metastasis are associated with degradation of components of the extracellular matrix by different proteinases. Among those, papain-like cysteine proteases, such as cathepsin B, seem to play an important role, as they are associated with poor clinical outcome in different cancers. In this study, we tested whether cystatin C, a natural extracellular inhibitor of papain-like cysteine proteases, can inhibit metastasis when overexpressed at the tumor-host interface. Local overexpression of cystatin C in liver and lungs of CD1 nu/nu mice was achieved by gene transfer with a novel adenoviral construct, which also led to the presence of 60 ng/mL of cystatin C in the serum. Three days after gene transfer, these mice were challenged by i.v. inoculation of lacZ-tagged human fibrosarcoma cells (HT1080lacZ-K15), leading to the formation of experimental lung and liver metastases. In this model, formation of experimental metastatic foci correlated with expression of cathepsin B in lungs, whereas there was no correlation with metastasis to the liver. In mice overexpressing cystatin C, the number of lung metastases was significantly reduced by 92%, as compared with mice receiving control adenovirus. The efficacy of extravasation of HT1080lacZ-K15 cells into the liver was not affected, indicating the independence of this process from the activity of cysteine-cathepsins. The present report is the first evidence of successful reduction of metastasis by inhibition of cysteine-cathepsins by cystatin C overexpression in the host microenvironment. Furthermore, organ-specific protease expression during tumor-host cell interactions could affect the success of antiproteolytic intervention against metastasis.

Adenoviridae↗
PubMed2005

Unexpected effect of matrix metalloproteinase down-regulation on vascular intravasation and metastasis of human fibrosarcoma cells selected in vivo for high rates of dissemination.

The human tumor/chick embryo model involving grafting of human HT-1080 fibrosarcoma cells on the chorioallantoic membrane was used in conjunction with quantitative real-time Alu PCR to select in vivo a pair of isogenic cell lines (HT-hi/diss and HT-lo/diss), dramatically differing in their ability to disseminate from the primary tumor (i.e., intravasate into the chorioallantoic membrane vasculature and metastasize to the lungs). During an immunohistochemical time course study, HT-hi/diss cells were sequentially visualized having escaped from the primary tumors, engaged with the blood vessels, and eventually observed inside the chorioallantoic membrane capillaries, thus reflecting early intravasating events. In contrast, HT-lo/diss cells seemed restricted to their primary tumor. Importantly, after i.v. inoculation, both variants arrested, extravasated, and proliferated in host tissues with similar efficiencies, highlighting that the observed earlier events at the periphery of the primary tumor could account for their differential dissemination. In a mechanistic probing of these events, we determined that HT-hi/diss intravasation was sensitive to a broad-range matrix metalloproteinase (MMP) inhibitor. To analyze the possible role of individual MMPs, membrane-bound MMP-14 and secreted MMP-9 were individually down-regulated in HT-hi/diss cells with their corresponding small interfering RNAs. Despite efficient down-regulation of MMP-14, neither intravasation nor metastasis of HT-hi/diss cells was affected significantly. However, a substantial down-regulation of MMP-9 was accompanied by a surprising 3-fold increase in intravasation and metastasis. The results emphasize a rising awareness that targeting certain MMPs might result in an enhanced malignancy, exemplified herein at the intravasation level as this step of the metastatic cascade is dissected and quantified.

Animals↗
PubMed2006

Transforming growth factor-beta1 induces tissue inhibitor of metalloproteinase-1 expression via activation of extracellular signal-regulated kinase and Sp1 in human fibrosarcoma cells.

The net balance of matrix metalloproteinases (MMP) and tissue inhibitor of metalloproteinases (TIMP) system has been known to be a key factor in tumor cell invasion. In the present study, we investigated the molecular mechanisms of anti-invasive and antimigrative activity of transforming growth factor (TGF)-beta1 on HT1080 human fibrosarcoma cells. In in vitro Matrigel invasion and Transwell migration assays, TGF-beta1 dose-dependently inhibited the invasion and migration of HT1080 cells, respectively. Gelatin zymography, Western blot, and real-time PCR analysis showed that TGF-beta1 enhanced the expression and secretion of MMP-2, TIMP-1, and, to a lesser degree, MMP-9 but not membrane type 1-MMP and TIMP-2. The addition of recombinant TIMP-1 protein reduced the Matrigel invasion and Transwell migration of HT1080 cells, similar to TGF-beta1. Because augmentation of TIMP-1 might be the major factor for the anti-invasive and antimigrative activity of TGF-beta1, we investigated possible molecular mechanisms responsible for the expression of TIMP-1 induced by TGF-beta1. Treatment of HT1080 cells with TGF-beta1 rapidly phosphorylated three mitogen-activated protein kinases [MAPK; extracellular signal-regulated kinase 1/2 (ERK1/2), p38, and c-Jun NH2-terminal kinase] and Akt. Among these kinases, the inhibition of only ERK1/2 pathway by PD98059, a specific inhibitor of MAPK/ERK kinase(MEK)-1, and transfection of dominant-negative MEK 1 effectively blocked the TIMP-1 induction by TGF-beta1. Mithramycin, a specific inhibitor of Sp1 transcription factor, but not curcumin, an inhibitor of activator protein-1, and transfection of Sp1 small interfering RNA significantly inhibited the TGF-beta1-induced expression of TIMP-1. In addition, electrophoretic mobility shift assay showed that TGF-beta1 up-regulated Sp1 DNA-binding activity, and PD98059 and mithramycin effectively inhibited these events. Finally, pretreatment of HT1080 cells with PD98059 and mithramycin, but not curcumin, restored the invasive activity of these cells. Taken together, these data suggest that TGF-beta1 modulates the net balance of the MMPs/TIMPs the systems in HT1080 cells for anti-invasion and antimigration by augmenting TIMP-1 through ERK1/2 pathway and Sp1 transcription factor.

Cell Movement↗
PubMed2001

Inoculation of human interleukin-17 gene-transfected Meth-A fibrosarcoma cells induces T cell-dependent tumor-specific immunity in mice.

OBJECTIVE: The biological activities of interleukin-17 (IL-17), a newly cloned cytokine, have not been fully elucidated. The present study was designed to assess the in vitro and in vivo effect of transfecting the IL-17 gene into tumor cells. METHODS: A complementary DNA (cDNA) encoding human IL-17 (hIL-17) was obtained by polymerase chain reaction amplification from the human CD4+ T cell cDNA library and inserted into the plasmid pRc/cytomegalovirus to construct an expression vector for the hIL-17 gene. Murine Meth-A fibrosarcoma cells were transfected with the hIL-17 gene using the lipofectin method. The hIL-17 gene-expressing clone (Meth-A/IL-17) was selected and analyzed for cytokine expression by Northern blot. RESULTS: There was no significant difference in the in vitro proliferation rate among parent Meth-A, cells transfected with vector alone and Meth-A/IL-17 cells. When the tumor cells were transplanted subcutaneously into BALB/c nude (nu+/nu+) mice, there was no difference in in vivo growth rates among the three cell lines. Challenge with tumor cells in conventional BALB/c mice, however, resulted in the rejection of Meth-A/IL-17 cells, but the other two lines did grow. After immunization with Meth-A/IL-17 cells, the mice were rechallenged by parent Meth-A or syngeneic MOPC-104E plasmacytoma cells; the immunized mice rejected the Meth-A cells, but not the MOPC-104E cells. Injecting the anti-thy 1,2 (CD90), anti-CD4 or anti-CD8 monoclonal antibody into conventional BALB/c mice resulted in the resumption of in vivo growth of Meth-A/IL-17 cells, but injecting the anti-asialo GM1 antibody did not. Furthermore, flow cytometric analysis demonstrated a significant increase in the expression of major histocompatibility complex (MHC) class I and class II antigens and lymphocyte function-associated antigen-1 on Meth-A/IL-17 cells. CONCLUSION: Meth-A cells transfected with the hIL-17 gene can induce tumor-specific antitumor immunity by augmenting the expression of MHC class I and II antigens, and both CD4+ and CD8+ T cells may play important roles in inducing antitumor immunity, suggesting the possibility of developing a tumor vaccine incorporating IL-17-transfected tumor cells.

Animals↗
PubMedDate not supplied

Establishment and characterization of clonal cell lines derived from a fibrosarcoma of the H2-K/V-JUN transgenic mouse. A model of H2-K/V-JUN mediated tumorigenesis.

We used fibrosarcoma from an H2-K/V-JUN transgenic mouse to derive a series of three immortal cell lines (JUN-1, -2, and -3). The cell lines exhibit strikingly different behavior regarding phenotype transformation. Features examined include contact inhibition and density limitation of growth, proliferation, invasiveness, motility, and organization of the microfilament system. Overall, JUN-2 and JUN-3 represent extreme phenotypes, with JUN-2 having a phenotype indicative of low-level cellular transformation and JUN-3 meeting all the criteria of the transformed phenotype. JUN-1 cells can also be regarded as transformed, but to a lesser extent than JUN-3. Their phenotype is in the majority of characteristics intermediary between JUN-2 and JUN-3. The transformation status is inversely related to the expression of the V-JUN transgene, which is the highest in JUN-2, lower in JUN-1 and very low in JUN-3. This might be related to the MHC class I promoter driving its expression and to the general observation of repression of MHC class I genes coupled with cellular transformation. Based on this premise, we present a model of H2-K/V-JUN-mediated tumorigenesis, in which v-jun-conditioned transformation represents merely an initial phase of tumorigenesis. Later during tumor progression, additional oncogenes are activated and/or tumor suppressor genes inactivated, leading on the one hand to further exacerbation of the transformed phenotype, and on the other hand to the repression of the H2-K/V-JUN transgene (fixed in JUN-3). We believe that the system of JUN cell lines can be valuable for further molecular analysis of transformation-related traits.

Actins↗
PubMedDate not supplied

Combined prenatal ultrasound and magnetic resonance imaging in an extensive congenital fibrosarcoma: a case report and review of the literature.

OBJECTIVE: Tumors of congenital origin differ in their symptoms and signs, predominant location and prognosis from those occurred later in childhood. To determine whether the prognosis of congenital (infantile) fibrosarcoma in the retroperitoneum, an extremely rare form of soft tissue malignant tumor, can be assessed prenatally. METHODS: We describe a case of this condition diagnosed in utero, including the assessment of the tumor behavior by ultrasound and magnetic resonance imaging. We also review the English language literature in Medline over the past 10 years and describe the management options available in such cases. RESULTS: Our case had precise prenatal findings revealed unfavorable conditions such as bulky tumor mass, spinal metastasis and pulmonary hypoplasia. CONCLUSION: Fetal imaging studies could accurately identify the invasion of tumor. The outcome is usually poor, especially for those fetuses affected by an axial location of the tumor.

Adult↗
PubMed1997

Effects of 1,25-dihydroxyvitamin D3 on tumor cell invasion to the extracellular matrix in human fibrosarcoma HT1080 cells and its correlation with laminin.

We investigated the role of the active form of vitamin D, 1,25-dihydroxyvitamin D3[1,25(OH)2D3], in promoting tumor cell invasiveness through the extracellular matrix, and showed that 1,25(OH)2D3-induced reduction of laminin production by the cells was correlated with the inhibitory effect of the hormone on tumor cell invasiveness. 1,25(OH)2D3 significantly inhibited invasiveness through the matrix, type IV collagenolytic and migratory activity, but not cell attachment to the matrix in human fibrosarcoma HT1080 cells. The 1,25(OH)2D3-induced inhibition showed the same dose dependency and magnitude for invasiveness as for the effects on type IV collagenolysis and cell migration. 1,25(OH)2D3 inhibited laminin production from the cells in a dose-dependent manner. The inhibitory effects of 1,25(OH)2D3 on the invasiveness, type IV collagenolysis and cell migration appeared to parallel the hormone-induced reduction of laminin production. Antilaminin monoclonal antibody, blocking the activity of laminin in the culture medium, inhibited HT1080 cell invasiveness. In the presence of exogenous laminin, 1,25(OH)2D3-induced inhibition of invasion was not observed. These findings suggest that 1,25(OH)2D3 acts on HT1080 cells, inhibiting the expression of laminin from the cells, and that the reduced laminin expression leads to the inhibition in the type IV collagenolytic and migratory activity of the cells, and consequently, to the inhibition of invasiveness through the extracellular matrix.

Calcitriol↗
PubMed1982

CAMP differences between clones of high and low malignant fibrosarcoma cells.

The levels of 3',5'-cyclic adenosine monophosphate (cAMP) were measured in a high malignant and a low malignant clone of murine fibrosarcoma cells isolated from a common parent in a normal mouse fibroblasts at various stages of growth. There was an inverse correlation between the degree of malignant potential and the cAMP levels. The normal fibroblasts had the highest cAMP at all time periods measured. The high malignant cells had the lowest levels and the low malignant cells were intermediary. The degree of susceptibility of each population to the growth inhibiting effects of dibutyryl cAMP, a cAMP analogue, was also measured. There was a direct correlation between degree of malignant potential and susceptibility to growth inhibition. These findings strongly support our belief that the low malignant cells represent a state of malignancy that is intermediary between the high malignant cells and the normal fibroblasts. cAMP differences may contribute to this.

Animals↗
PubMed1992

Differences in cellular proteins between high and low metastatic potential sublines from the methylcholanthrene-induced rat fibrosarcoma cell line.

The purpose of the present study was to determine with two-dimensional electrophoresis whether two sublines (high and low metastatic potential to lymph nodes) of rat fibrosarcoma induced by methylcholanthrene have differences in cellular proteins. The high metastatic potential subline had a specific protein in the protein map of the whole cell lysate. Its isoelectric point was 6.4 and the molecular weight was 18,000. This specific protein appeared in maps of the precipitate of 1,000 g centrifugation and in the supernatant from treatment with 0.5% Nonidet P-40 (NP-40). But this specific protein was not stained by five lectins, concanavalin A, wheat germ agglutinin, Ulex europeus agglutinin-1, Dolichis biflorus agglutinin, and Ricinus communis agglutinin. Apparently, this high metastatic potential subline has a specific protein in the plasma membrane which has no glycochain.

Animals↗
PubMedDate not supplied

Purpurogallin inhibits DNA synthesis of murine fibrosarcoma L-929 and human U-87 MG glioblastoma cells in vitro.

We demonstrated, for the first time, that the flavonoid purpurogallin (PPG) at 0.2-0.5 mM inhibits DNA synthesis of murine fibrosarcoma L-929 and human U-87 MG glioblastoma cells in vitro. In the human U-87 MG glioblastoma cell experiments, we found that when cells were incubated with PPG at 0.5 mM for 0.5 and 24 h, about 25 and 50% inhibition of DNA compared with control were observed respectively. In contrast, 0.5 mM Trolox (a more polar analogue of vitamin E) did not inhibit DNA synthesis in both cell lines. These data indicate that PPG inhibits the synthesis of DNA in two distinct tumour cell lines.

Antioxidants↗