Disease relevance of Fibrosarcoma

• MSA and EGF receptors on sarcoma virus transformed cells and human fibrosarcoma cells in culture [1].
• B16 and K-1735 subcutaneous (s.c.) tumors producing high levels of GM-CSF significantly suppressed lung metastasis of 3LL, UV-2237 fibrosarcoma, K-1735 M2, and B16-F10 cells, but parental or low-producing tumors did not [2].
• Synthesis and cell surface expression of gp130 were greatly increased in both virally and chemically transformed fibroblasts, fibrosarcomas, a squamous cell carcinoma of the skin, and T cell leukemia lines [3].
• Moreover, the up-regulation of NKG2D ligands by E1A was not limited to mouse tumor cells, as E1A also increased the expression of NKG2D ligands on primary baby mouse kidney cells, human MB435S breast cancer cells, and human H4 fibrosarcoma cells [4].
• TSP binding to C32 melanoma cells and HT1080 fibrosarcoma cells was specific and also inhibitable with OKM5 Mab [5].

High impact information on Fibrosarcoma

• A novel ETV6-NTRK3 gene fusion in congenital fibrosarcoma [6].
• Neovascularization is associated with a switch to the export of bFGF in the multistep development of fibrosarcoma [7].
• To investigate whether the activated N-ras oncogene of HT1080 human fibrosarcoma cells contributes to the expression of the transformed phenotype, we have isolated flat revertants [8].
• When treated with the synthetic glucocorticoid dexamethasone, HT1080 human fibrosarcoma cells show changes in morphology, adhesion, and the extracellular matrix [9].
• The murine fibrosarcoma cell line HSDM1C1 synthesizes prostaglandin E2 in response to thrombin and bradykinin, two products of the coagulation pathway [10].

Chemical compound and disease context of Fibrosarcoma

• Hydrocortisone inhibits prostaglandin production by mouse fibrosarcoma cells [11].
• Tumor necrosis factor/cachectin-induced intravascular fibrin formation in meth A fibrosarcomas [12].
• Low-dose cyclophosphamide inhibition of transplantable fibrosarcoma growth by augmentation of the host immune response [13].
• In an attempt to improve the antitumor efficacy of bleomycin, the effects of the oxygen-carrying emulsion Fluosol-DA and increased levels of inspired oxygen were tested in the mouse FSaIIC fibrosarcoma system [14].
• To examine further the role of arachidonic acid conversion to prostaglandins (PG) in hypercalcemic mice bearing the PG-producing HSDM1 fibrosarcoma, we have performed experiments in which control and tumor-bearing animals were fed diets either low (0.1-0.2% of total fatty acid) or high (17%) in EPA [15].

Biological context of Fibrosarcoma

• A mutant form of the alpha-isoform of protein kinase C (PKC) was recently isolated from an ultraviolet radiation-induced murine fibrosarcoma cell line and reported to transform mouse BALB/c 3T3 fibroblasts on transfection [16].
• The DNA's from two of four methylcholanthrene-induced mouse fibrosarcomas contained transforming genes that were identical in their pattern of restriction endonuclease resistance to inactivation of biologic activity [17].
• Human rTNF/Cachectin was shown to stimulate gene transcription of plasminogen activator inhibitor (PA1)-1 and PAI-2, and simultaneously suppress constitutive gene expression of tissue-type plasminogen activator (t-PA) in human fibrosarcoma cells [18].
• METHODS: Expression plasmids containing either the neomycin-resistance gene and the complementary DNA sequence encoding human cyclin D1 or the neomycin-resistance gene only (control) were transfected by lipofection into the human HT1080 fibrosarcoma cell line, and cell colonies resistant to the antibiotic neomycin (G418) were isolated [19].
• Down-regulation of murine fibrosarcoma transforming growth factor-beta 1 expression by interleukin 7 [20].

Anatomical context of Fibrosarcoma

• Supernatants of cultured meth A fibrosarcomas obtained serum-free conditions, which had no intrinsic procoagulant activity, considerably enhanced tissue factor induction in endothelium in response to submaximal concentrations of TNF [12].
• In the present study, we demonstrate that alteration of the metalloproteinase-metalloproteinase-inhibitor balance in favor of excess inhibitor blocks human fibrosarcoma HT-1080 tumor cell invasion of a reconstituted basement membrane [21].
• Inhibition by bovine endothelial cells of degradation by HT-1080 fibrosarcoma cells of extracellular matrix proteins [22].
• The nonionic detergent octyl-beta-D-glucopyranoside (C8Glu) was used to extract immunogenic tumor-specific transplantation antigen (TSTA) from intact cells and purified plasma membranes of the 3-methylcholanthrene-induced fibrosarcoma MCA-F [23].
• Conversely, tumor cell expression of NCAM in a fibrosarcoma model (T241) improved pericyte recruitment and increased perivascular deposition of ECM molecules [24].

Gene context of Fibrosarcoma

• RESULTS: A variety of drug-resistant human cancer cell lines derived by selection with mitoxantrone markedly overexpressed BCRP mRNA; these cell lines included sublines of human breast carcinoma (MCF-7), colon carcinoma (S1 and HT29), gastric carcinoma (EPG85-257), fibrosarcoma (EPF86-079), and myeloma (8226) origins [25].
• Three of these tumours, a T-cell lymphoma, a fibrosarcoma and a macrophage tumour, were found to carry an activated c-Ki-ras gene [26].
• HFKs, HT1080 fibrosarcoma and QG56 cells, as well as many other human cells, contain varying ratios of GP90 and structurally related, higher molecular mass forms of CD44 that express the following characteristics: (a) each form reacted with anti-CD44 (mAbs) P1G12, P3H9, and P3H5 [27].
• Human TCP1 cDNA clones from both fibrosarcoma and B cell lines confirmed that there was a single expressed gene. mRNA transcripts of different sizes were accounted for by two different polyadenylation signals [28].
• The E-26 transforming specific (ETS)-related gene TEL, also known as ETV6, is involved in a large number of chromosomal rearrangements associated with leukemia and congenital fibrosarcoma [29].

Analytical, diagnostic and therapeutic context of Fibrosarcoma

• Four groups of female C57BL/6 mice with pulmonary metastases from a 3-methylcholanthrene-induced fibrosarcoma (MCA-105) and four groups of nontumored mice were treated every 6 h for 4 d by intraperitoneal injections of either IL-2 alone, IL-2 and PTXF, PTXF alone, or equal volumes of saline [30].
• When administered to athymic NCr-nu/nu mice bearing 1-cm diameter human fibrosarcoma HT-1080 xenografts, the labeled antibody preferentially localized in tumor deposits [31].
• Oral administration of beta-carotene (120 micrograms/mouse/day) for 9 days from day 1 to the BALB/c mice inoculated sc with 10(7) syngeneic BALB/c Meth A fibrosarcoma cells (Meth A) led to a remarkable rejection against rechallenged Meth A implanted sc on day 10 [32].
• Metastatic behavior of the RIF-1 murine fibrosarcoma: inhibited by hypophysectomy and partially restored by growth hormone replacement [33].
• We have used quantitative electron microscope autoradiography to study uptake and distribution of arachidonate in HSDM1C1 murine fibrosarcoma cells and in EPU-1B, a mutant HSDM1C1 line defective in high affinity arachidonate uptake [34].

References