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PubMed1979

[Hematopoiesis and changes in the RES of the spleen pulp in fibrosarcoma-bearing rats].

The transplantable fibrosarcoma of the Rat gives birth to different modifications in the splenic structures, and a strong perturbation is found within the enzymatic activities. The macrophages have an altered acid phosphatase activity. This is in marked contrast to the increase in number of the alkaline phosphatase polymorphonuclear cells, which are originated from myeloid areas in the red pulp. Lymphoïd-reticular cells, possessing one 5'nucleotidase activity, seem to be responsible, possibly, by forming numerous clonal systems during the development of this fibrosarcoma. The role of this separate system is discussed.

5'-Nucleotidase↗
PubMed1989

Tumorigenic latency and separable stages during fibrosarcoma development in transgenic mice carrying papillomavirus genomes.

Transgenic mice have been established carrying the genomes of bovine papillomavirus type 1 (BPV-1), and human papillomaviruses types 5 and 18. Transcriptional dormancy is characteristic of all three viral genomes in transgenic mouse lines maintained for 2-4 years. Only BPV-1, which induces both dermal and epidermal pathology in its natural host, has been found to elicit abnormalities when carried in transgenic mice. The BPV-1 genome acts in these mice as a tissue specific oncogene, in that it elaborates the development of skin fibrosarcomas. Three abnormal stages are evident: two distinct and successive stages of a proliferative hyperplasia (a mild and an aggressive fibromatoses), and the solid tumors (fibrosarcomas). Analysis of tissue biopsies and of derivative cell cultures from each pathology confirms that this pathway is composed of separate stages. Notably, progression from hyperplasia to neoplasia is accompanied by specific cytogenetic changes, which appear necessary in addition to the actions of the BPV oncogenes. The reproducibility of the tumorigenic pathway induced by the BPV genome is providing inroads into the molecular genetic and biochemical mechanisms of tumor development.

Animals↗
PubMed1989

Immunogenicity of a soluble partially purified oncofetal antigen from murine fibrosarcoma in syngeneic mice.

A tumor/fetal associated antigen, termed oncofetal antigen (OFA), conserved in the tumor and fetal tissue of rodents and humans, was extracted from murine fibrosarcoma cells and tumors and was fractionated on an Ultrogel AcA34 gel filtration column. A monoclonal antibody 115 specific for the OFA identified three peaks of antigenic activity in the eluted fractions, designated fractions (Fr.) I, II, and III, in the molecular weight range of greater than 160, 90, and 44 kDa, respectively. Most of the activity resided in the high molecular weight fraction, Fr. I. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis analysis and gel scanning of Fr. I showed multiple bands, one of which, constituting about 5.6% of the total protein bands in Fr. I, was the 44 kDa oncofetal antigen, apparently present in this fraction in a soluble complex form. Lectin binding studies and isoelectric focusing showed that the 44 kDa OFA is a glycoprotein, whose pI is 6.8. Spleen and peritoneal exudate cells of BALB/c mice immunized with Fr. I protected naive syngeneic mice, in adoptive transfer experiments, from developing tumors when challenged with syngeneic fibrosarcoma tumor cells, MCA-1315. Also, immune spleen cells were cytotoxic to the tumor target cells, MCA-1315, in a 51Cr release assay at several different effector to target cell ratios. This is the first description of a conserved, true, oncofetal antigen capable of inducing tumor transplantation resistance in syngeneic rodents in a semipurified form.

Animals↗
PubMed1989

[A case of retroperitoneal fibrosarcoma].

A case of retroperitoneal fibrosarcoma is reported. An 81-year-old man was admitted to our hospital with gross hematuria. X-ray examination of intravenous pyelography, computed tomography and angiography revealed left hydronephrosis and left renal tumor. Excisional surgery was carried out. The tumor and left kidney were completely removed. Pathological diagnosis was retroperitoneal fibrosarcoma. Five months later, he died of lung and liver metastasis.

Aged↗
PubMed1989

[Pericardial fibrosarcoma demonstrated by Ga-67 scintigraphy].

A case of malignant fibrosarcoma originated from pericardium was reported. A 31 year-old female who complained of general fatigue and back pain showed dilated cardiac shadow in chest X-ray. Cardiac blood pool scan with 99mTc-RBC revealed avascular mass in pericardial cavity which push the heart up and left side. It was suspected to be malignant, since the mass had increased 67Ga uptake. CT and MRI also demonstrated that the tissue characterization of the pericardial mass was irregular, and the mass compressed venous return. The large mass originated from pericardium caused the right sided cardiac failure. In 12 years ago, she had a history of operation which resected benign hemangioma in the same space (pericardium). We could suspect the malignant transformation between the two rare pericardial tumors; benign hemangioma and malignant fibrosarcoma.

Adult↗
PubMed1988

[Correlation between intracellular cyclic AMP level and cytotoxic sensitivity to anti-tumor-associated antigen antibody in rat fibrosarcoma cells].

We investigated the intracellular cyclic AMP (cAMP) level and cytotoxic sensitivity to anti-tumor-associated antigen (anti-TAA) antibody in transplantable rat fibrosarcoma cells with regard to each of three days following ip transplantation. The cytotoxic sensitivity of the 3-methylcholanthrene (MCA)-induced transplantable fibrosarcoma KMT-17 cells to anti-TAA antibody decreased daily after ip transplantation in syngeneic WKA/Hok rats. In contrast, the intracellular cAMP level of the tumor cells increased daily after ip transplantation, and the cAMP level of 3-day-old KMT-17 tumor cells (1.31 pmol/10(6) cells) was statistically (p less than 0.01) higher than that of 1-day-old tumor cells (1.01 pmol/10(6) cells). This phenomenon disappeared, however, after artificial infection of the tumor cells with Friend murine leukemia virus (F-MuLV). The cytotoxic sensitivity of F-MuLV-infected KMT-17 (FV-KMT-17) tumor cells to anti-TAA antibody did not decrease and no elevation of the intracellular cAMP level was observed (0.92-0.97 pmol/10(6) cells), regardless of the number of days after ip transplantation. The cytotoxic sensitivity of KMT-17 and FV-KMT-17 tumor cells to anti-TAA antibody was therefore in inverse proportion to the intracellular cAMP levels of the tumor cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

[Fibrosarcoma: immunohistochemical study of the extracellular matrix].

Immunofluorescent examination of extracellular matrix of 5 fibrosarcomas showed the matrix to contain fibronectin and collagen type I, III, V. Fibrosarcoma matrix is characterized by the absence of collagen type IV and collagen type III predominance over type I differentiating this tumor from synovial sarcoma, neurogenic sarcoma, dermatofibrosarcoma protuberans, malignant fibrous histiocytoma. Their matrices showed the presence of type IV collagen, equal proportion of interstitial collagens or collagen type I predominance over type III typical for synovial sarcoma. The findings can be employed in practical morphologic diagnosis of soft tissue tumors.

Collagen↗
PubMed1988

Mass quantitation of agonist-induced arachidonate release and icosanoid production in a fibrosarcoma cell line. Effect of time of agonist stimulation, amount of cellular arachidonate, and type of agonist.

The mass of total arachidonate released from phospholipids upon agonist stimulation of the cell and the fraction of released arachidonate which is converted to icosanoids are two parameters of arachidonate metabolism which have been difficult to quantitate because the mass of arachidonate released upon cell stimulation is very low. We have been able to quantitate both of these parameters under a variety of experimental conditions using a unique essential fatty acid-deficient mouse fibrosarcoma cell line (EFD-1), which when repleted with arachidonate, produces prostaglandin E2 (PGE2). Because there is no endogenous pool of arachidonate in these cells, the specific activity of exogenous arachidonate does not change upon incorporation into cells, an advantage which permits mass determination of very small quantities of arachidonate directly from radioactive counts. EFD-1 cells were incubated with various concentrations of [14C]arachidonate (for release studies) or unlabeled arachidonate (for PGE2 radioimmunoassays) for 24 h and then stimulated with bradykinin. The time courses for arachidonate release and PGE2 production demonstrated that free arachidonate was rapidly converted to PGE2 with plateau levels attained for both parameters within 240 s of agonist exposure for 2 microM and for 10 microM arachidonate-repleted cultures. There was a linear relationship (r = 0.94) between the mass of arachidonate in the cell and the mass of arachidonate released upon stimulation, up to a cellular concentration of 11 nmol of arachidonate/10(6) cells, a concentration 10-20% above normal for the parent mouse fibrosarcoma cell line (HSDM1C1) which is not essential fatty acid-deficient. Importantly, the percent of released arachidonate which was converted to PGE2 decreased from 90 to 15% with increasing concentrations of cellular arachidonate, because PGE2 production plateaued at greater than or equal to 6 nmol of arachidonate/10(6) cells, but total arachidonate release continued to rise. Finally, we demonstrated that agonist stimulation with thrombin, A23187, and bradykinin all showed the same percent conversion of released arachidonate to PGE2, implying that the determination of this fraction is not a function of the mechanism of release. These studies with our unique cell line indicate that, when the concentration of arachidonate in the cell is not elevated above amounts normally found in our HSDM1C1 cell line, released arachidonate is rapidly and almost quantitatively converted to PGE2, independent of the agonist used to stimulate the cells.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1988

Glucocorticoid-induced alterations of morphology and growth of fibrosarcoma cells derived from 7,12-dimethylbenz(a)anthracene rat mammary tumor.

Cloned cell strains with adverse patterns of differentiation obtained from 7,12-dimethylbenz(a)anthracene-induced rat mammary tumor tissue were used to study the effects of glucocorticoid hormones on morphology and proliferation. HH-16 clone 2/1 cells apparently reflecting mesenchymal cells of the stromal part of the mammary gland grow as elongated, mostly bipolar fibroblasts in criss-cross patterns. When cultured in the presence of glucocorticoids, the cells flattened, lost bipolarity, extended in size, and showed arrest of growth at confluence, possibly due to contact inhibition. Immunocytochemical examination of dexamethasone-treated cells revealed actin cables which were absent in untreated cells. The hormone-treated cells expressed Mr 50,000-67,000 cytokeratins, and the extracellular matrix proteins fibronectin and laminin were increased. The in vitro effects on morphology and growth were reversible 3-4 days after withdrawal of the glucocorticoids. In dexamethasone-treated animals the growth of fibrosarcomas produced by inoculation of newborn rats with HH-16 clone 2/1 cells was reduced, and the survival time of the tumor-bearing animals was extended. Apparently, morphology and growth of HH-16 clone 2/1 fibrosarcoma cells can be controlled by glucocorticoids. In comparison, epithelioid HH-16 clone 4 cells established simultaneously from 7,12-dimethylbenz(a)anthracene-induced rat mammary tumor were unresponsive to glucocorticoids.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1988

Functional role of platelets in experimental metastasis studied with cloned murine fibrosarcoma cell variants.

The involvement of platelets in experimental metastasis was studied with cloned cell lines derived from PAK 17, a recently induced methylcholanthrene-induced C57BL/6 mouse fibrosarcoma. Tumor cell-induced platelet aggregation and lung colonization assays were used to distinguish three major stable phenotypes among the clones: a low metastatic-low platelet aggregating type, e.g., clone PAK 17.12; a low metastatic-high platelet aggregating type, e.g., clone PAK 17.14; and a high metastatic-high platelet aggregating phenotype, e.g., clone PAK 17.15. Clones with high metastatic but low platelet aggregating potential were not observed in the study. Intravenously injected PAK 17.14 and PAK 17.15 cells, but not PAK 17.12 cells, induced greater than 50% reductions in circulating platelet levels in C57BL/6 mice. Since highly metastatic clone PAK 17.15 cells consistently induced high levels of tumor cell-induced platelet aggregation regardless of the platelet donor, it was selected to study the relationship between its tumor cell-induced platelet aggregation and lung colonizing abilities. (a) A 93% decrease in lung colony number resulted in mice injected with 100 micrograms of prostacyclin immediately before injection of clone PAK 17.15 cells. Prostacyclin was also able to inhibit, in a dose dependent fashion (0-5 ng), platelet aggregation induced by clone PAK 17.15 cells in vitro. (b) A 92% reduction in lung colony number occurred in mice showing marked thrombocytopenia following injection of 100 micrograms of rabbit anti-mouse platelet antibody 24 h before tumor cell injection. (c) A greater than 80% reduction in clone PAK 17.15 lung colony number was observed in mice rendered thrombocytopenic by i.v. injection of 0.038 units of neuraminidase 24 h before i.v. injection of 10(5) tumor cells. These results suggest that platelets are required for successful lung colonization by clone PAK 17.15 cells. However, the presence in this fibrosarcoma of high platelet aggregating-poorly metastatic cells, such as clone PAK 17.14, demonstrates that while the ability to aggregate platelets is necessary for successful metastasis by some tumor cells, it is insufficient if tumor cells lack other critical properties required for completion of the metastatic cascade.

Animals↗
PubMed1988

Site-specific metastasis of mouse melanomas and a fibrosarcoma in the brain or meninges of syngeneic animals.

Different subpopulations of cells from two different murine melanomas (K-1735 and B16) and a fibrosarcoma (UV-2237) were injected into the internal carotid artery of anesthetized syngeneic mice. Despite the common route of tumor cell injection, tumor lesions in the brain were unique to each tumor type and developed at different sites in the brain. Gross and histological examinations revealed that different subpopulations of cells derived from the K-1735 melanoma produced only parenchymal lesions, cells of the B16 melanoma produced lesions in the meninges and ventricles, and cells of the UV-2237 fibrosarcoma produced lesions throughout the brain. This site specificity for tumor growth was not due to the initial tumor cell arrest in the microvasculature of different regions-areas in the brain as evidenced by detailed studies with radiolabeled cells. The site specificity of this experimental brain metastasis was not random and correlated well with the clinical situation. The exact interactions of tumor cells with different microenvironments in the brain need further elucidation.

Animals↗
PubMed1988

Anti-tumor activity of recombinant tumor necrosis factor on mouse fibrosarcoma in vivo and in vitro.

The experiments presented were designed first to determine the effects of rTNF on the methylcholanthrene-induced fibrosarcoma (FSA-1) in C3H/JSed mice and second to determine whether the observed effects are the result of direct action by rTNF on the tumor or whether rTNF acts as a mediator of other effector mechanisms. Mice received syngeneic FSA-1 fibrosarcoma cells either s.c. or i.v. in order to evaluate growth of transplantable solid tumor or lung metastases, respectively. The range of dosages, from 10(2) to 2 x 10(5) U of rTNF, was administered i.v. at different intervals after the tumor cell injection. Early injection of 10(3) to 10(4) U of rTNF reduced the growth of s.c. injected tumor and the number of lung metastases in i.v. injected mice. In both cases, survival of mice was also prolonged. However, in vitro treatment of FSA-1 tumor cells with rTNF did not result in the reduction of their proliferating activity after injection into mice, although direct cytostatic and moderate cytotoxic activity of rTNF in vitro was demonstrated. To identify whether other cellular mechanisms are involved in the effects observed in vivo, the anti-tumor activity of rTNF-treated spleen cells was evaluated in vitro using a 75Se release assay. Whereas nontreated spleen cells demonstrated very low cytotoxic activity in this system, the cells from rTNF-treated mice showed marked increase in the cytotoxicity against syngeneic tumor cells. These results suggest that the anti-tumor activity of rTNF represents a combination of its direct effect on tumor cells and indirect effects involving host immune mechanisms.

Animals↗
PubMed1986

[Antimetastasis effect of lymphokine-activated killer (LAK) cells on fibrosarcoma in WKA rats].

Treating WKA rats with fibrosarcoma with LAK cells, antimetastasis effect was studied. The results indicated that splenocytes incubated by IL-2 could produce lytic activity to WKA rats with fibrosarcoma in vitro. Passive infusion of LAK cells lead to a marked reduction in the number of metastatic nodules in the lung. After intravenous injection of LAK cells, cancer cells in the lung speedily disappeared. LAK cell administration for 3 times gave better result than once only (P less than 0.01). In this paper, the possibility of LAK cells used as an adoptive immunotherapy for human neoplasms is briefly discussed.

Animals↗
PubMed1986

[A case of giant hydronephrosis caused by renal fibrosarcoma].

The presented report is fibrosarcoma arising from renal capsule in a 64-year-old woman. The tumor is very rare and is the 25th case in Japan. The patient visited our hospital with the complaint of macroscopic hematuria for several days. Abdominal examination revealed a painless lump from the left lumbar region to para-median abdomen. A diagnosis of hydronephrosis caused by neoplasma or tuberculosis was considered by CT, AG, etc., and transperitoneal nephrectomy was performed on 6-July-1984. Pathology of the tumor was fibrosarcoma arising from the renal capsule. Three months later, the tumor was growing on the peritoneal surface from the left renal region and she died on Nov. 10, 1984.

Female↗
PubMed1987

Dynamic heterogeneity: characterization of two cell lines derived from experimental lung metastases of mouse KHT fibrosarcoma.

We have recently demonstrated that KHT fibrosarcoma variant cells that form experimental metastases are generated by a stochastic process at high effective rates (approximately 10(-5)/cell/generation). The metastatic variant cells are unstable and are rapidly lost with an effective rate of reversion of approximately 10(-1)/cell/generation. In this study, we have examined the dynamics of generation of metastatic variant cells for two lines of KHT cells derived from individual experimental lung metastases in a single step selection. When grown in vitro, the KHT35-L1 cell population maintained a highly metastatic phenotype whereas the KHT3-L1c cell population reverted to a poorly metastatic phenotype. Our results indicate that there is an approximately 10-fold higher effective rate of generation of metastatic variant cells for KHT35-L1 cells relative to KHT3-L1c cells. Thus, a higher effective rate of generation of metastatic variants accompanies a stably expressed metastatic ability in fibrosarcoma cells and, as we have previously reported, in melanoma cells.

Animals↗
PubMed1987

Nuclear magnetic resonance analysis of tumor necrosis factor-induced alterations of phospholipid metabolites and pH in Friend leukemia cell tumors and fibrosarcomas in mice.

The alterations induced on the pool sizes of five phospholipid metabolites, glycerol 3-phosphorycholine, glycerol 3-phosphorylethanolamine, phosphorylcholine, sn-glycerol 3-phosphate, and choline were studied by nuclear magnetic resonance (NMR) spectroscopy in murine tumors injected with recombinant murine tumor necrosis factor (TNF). Solid tumors were obtained by s.c. injection of either Friend leukemia cells (clones 3C1-8 and 745) in DBA/2 mice or murine fibrosarcoma cells (HeN4) in C3H/HeN mice. After tumor nodules had developed, TNF or bovine serum albumin was injected intratumorally. Treatment of both tumors with TNF resulted in a marked inhibition of tumor growth. 31P-NMR analyses of Friend leukemia cell tumors (and tissue extracts), 6 h after injection of TNF, showed: (a) a 1.5- to 3.5-fold decrease in the pool sizes of glycerol 3-phosphorylcholine and glycerol 3-phosphorylethanolamine; (b) a 7- to 8-fold increase of sn-glycerol 3-phosphate; (c) a 2- to 3.5-fold decrease of phosphorylcholine; (d) an alkaline shift (0.2 units) in intratumoral pH. Similar metabolic alterations occurred in TNF-treated HeN4 fibrosarcoma. 1H-NMR analyses of Friend leukemia cell tumor extracts also indicated, 6 h after tumor injection with TNF: (a) elevated choline levels (9X); (b) a 19-fold increase in the ratio [choline]/[phosporylcholine]; (c) elevated (1.4X) levels of lactic acid; and (d) a 1.6-fold decrease in the [taurine]/[glycine] ratio. The results are interpreted in the light of possible alterations in the activity of enzymes controlling the de novo biosynthesis and catabolism of phospholipids. We concluded that NMR spectroscopy can be a useful means to monitor the level of some phospholipid precursors and/or derivatives as early markers of therapeutic efficacy in intact neoplastic tissues.

Animals↗
PubMed1986

Effects of glucocorticoids on the growth of human fibrosarcoma cell line HT-1080.

The human fibrosarcoma cell line HT-1080 exhibits rapid growth following s.c. inoculation in 4-6-week-old male athymic mice. Cytosols from tumors carried in athymic mice bind glucocorticoid (Kd, 1.8 +/- 0.48 X 10(-8) M; Bmax, 240.5 +/- 35.3 fmol/mg cytosol protein, mean +/- SEM). Receptor sediments primarily in the 8-9S region on 5-20% sucrose gradients and is specific for the glucocorticoids. HT-1080 growth in vitro (as measured by cell count) was inhibited over a range of 10(-6)-10(-8) M after 7 days of incubation with dexamethasone and triamcinolone acetonide. Progesterone, estradiol, and dihydrotestosterone had no effect on HT-1080 growth in vitro. Preincubation with a 100-fold excess of progesterone reversed the growth inhibition observed with triamcinolone acetonide but not dexamethasone acetate. HT-1080 tumor cell growth responded biphasically to dexamethasone in vivo. Athymic mice given s.c. injections every other day with 5 or 25 micrograms dexamethasone showed an increase in tumor size inversely proportional to dose. In contrast, 200 micrograms of dexamethasone significantly inhibited tumor growth. Adrenalectomy did not significantly alter HT-1080 growth or glucocorticoid binding to tumor cytosols (Kd, 3.4 X 10(-8) +/- 1.1, Bmax, 236.9 +/- 9.9 fmol/mg cytosol protein, mean +/- SEM) although tumor incidence was decreased in sham adrenalectomized mice. Glucocorticoid binding in tumors grown in vivo was decreased by increasing amounts of dexamethasone. High pharmacological doses of glucocorticoids inhibit the growth of human fibrosarcomas in vivo and in vitro.

Adrenalectomy↗
PubMed1985

Regulation of plasminogen activator activity in human fibroblastic cells by fibrosarcoma cell-derived factors.

Low-molecular-weight protein factors (Mr 8,000 to 18,000) from serum-free conditioned medium of human fibrosarcoma (8387) cells reversibly enhanced the secretion of proteinase-inhibitory activity by cultured normal human skin fibroblasts. This inhibitory activity could be absorbed by immobilized plasminogen activator (PA) of urokinase type but not by heparin, and it was sensitive to treatment with sodium dodecyl sulfate. The secretion of a heparin-binding Mr 60,000 proteinase inhibitor, resembling protease nexin, was also detected. Early passages of adult skin fibroblasts do not contain or secrete PA. When cell types secreting this enzyme were tested, the fibrosarcoma-derived factors decreased the PA secretion detectable after sodium dodecyl sulfate treatment in all conditioned media of normal and malignant fibroblastic cells examined, including the 8387 cell line itself. However, no effects on the secretion of PA by normal or malignant cells of epithelioid origin or by melanoma cells were seen. A similar preparation from human epidermoid carcinoma (A431)-conditioned medium did not affect the PA activity or secretion of proteinase inhibitors from fibroblastic cells. The ability of sarcoma cells to modulate the production of PA inhibitors is a novel characteristic in the regulation of cellular proteolysis.

Cells, Cultured↗