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At least 145 records · Page 8Linked to original sources
PubMed1996

Infantile fibrosarcoma: complete excision is the appropriate treatment.

BACKGROUND: Infantile fibrosarcoma and its pathological variants are unusual childhood tumors. During the past 25 years, 18 children with these lesions were seen at our institution. METHODS: These patients' records were analyzed to determine clinical and pathological findings and outcome. RESULTS: The mean age at diagnosis was 7 months. There were 16 boys and 2 girls. The sites of tumor at presentation were: Extremity, head, trunk, and pelvis. Pathological findings were: fibrosarcoma, myofibroma, and fibromatosis. Histologic characteristics varied from benign hypocellular to more cellular pleomorphism. The initial surgical procedure was a complete excision in 16. Of those patients with complete removal, 6 recurred and all had secondary reexcision. In addition to excision, 3 patients received adjunctive therapy; chemotherapy in all 3 and radiation in 2. Sixteen (89%) children survived, including 4 of 6 with recurrent tumor and 2 of 2 with incomplete initial resection. Two children ages 6 and 9 months at diagnosis died of progressive recurrent tumor at 1 month and 6 years from initial diagnosis, despite operative therapy, chemotherapy, and radiation therapy. Both had paraspinal tumors that were removed completely. Pathological examination revealed spindle cell tumors infiltrating muscle. Neither clinical nor histologic findings distinguished surviving from nonsurviving patients. CONCLUSIONS: Fibrosarcoma occurring in infants has an excellent outcome despite histologic findings. Initial complete excision should be attempted in all children. Recurrence indicates a more aggressive variant and warrants more aggressive complete reexcision wherever possible. Adjunctive therapy probably has no benefit. The occasional death indicates the need for close follow-up.

Female↗
PubMed1997

Protective effect of magnesium supplementation on experimental 3-methyl cholanthrene-induced fibrosarcoma and changes in tissue magnesium distribution during carcinogenesis in rats.

In this study, we wanted to examine the effect of magnesium (Mg2+) supplementation on the experimental 3-methyl cholanthrene (3-MC)-induced fibrosarcoma and alterations in (Mg2+) distribution in several tissues of the rats, during carcinogenesis. It was determined that serum and tissue (Mg2+) levels of the rats in (Mg2+)-supplemented diet group were higher than those of the rats in the (Mg2+)-nonsupplemented and control groups. The mean time of fibrosarcoma development for (Mg2+)-supplemented group was longer than (Mg2+)-nonsupplemented group (p < 0.05). Symptoms of hypermagnesemia were not observed in any of the rats. These results suggests that dietary (Mg2+) supplementation may have a partial anti-carcinogenic effect on experimental 3-MC-induced fibrosarcoma by prolongation of the latent period of carcinogenesis.

Animals↗
PubMed2005

Primary giant congential infantile fibrosarcoma of the scalp: case report and review of literature.

CASE REPORT: A primary giant infantile fibrosarcoma of the scalp in a 6-month-old boy is reported. He presented with a rapidly enlarging right paramedian parietal scalp swelling since birth. There were no signs of raised intracranial tension. Magnetic resonance (MR) imaging of the brain revealed a large vascular scalp tumor extending over the posterior frontal and parietal region bilaterally crossing the midline. There was no intracranial extension. Carotid angiography revealed an extremely vascular tumor supplied by the external carotid artery branches. The tumor was completely resected through a curvilinear scalp incision. Histology was consistent with diagnosis of an infantile fibrosarcoma. The patient had an uneventful course and received no postoperative adjuvant therapy. MR imaging of the brain at follow-up after 5 years showed no evidence of recurrence of tumor. At follow-up after 10 years, he is asymptomatic and leading an active life. DISCUSSION: The pathology and management of primary scalp fibrosarcoma is discussed, and the relevant literature is briefly reviewed.

Fibrosarcoma↗
PubMed2004

Epithelioid fibrosarcoma of the ovary.

Recently, low-grade fibromyxoid sarcoma/hyalinizing spindle cell tumor with giant rosettes (LGMFS/HSCT) and sclerosing epithelioid fibrosarcoma (SEFS) have come to be recognized as distinctive types of fibrosarcoma. Because their pathological features seem to sometimes overlap, it may be that these tumors belong to a similar entity. We report an aggressive sarcoma with unusual histology arising from the right ovary of a 44-year-old woman. The tumor was 12 cm in size, and there were multiple distant metastases to lung, kidney, stomach and bones. Microscopically, the tumor was composed of broad sheets or variously sized nodules of polygonal epithelioid cells accompanied by hyalinous stroma, resembling SEFS. The hyalinous nodules surrounded by the palisading epithelioid cells, as seen in a rosette of HSCT, were scattered. Between these nodules, spindle cells arranged in fascicles or whorled bundles, mimicking LGMFS, proliferated. Immunohistochemical and ultrastructural analyses revealed fibroblastic differentiation of epithelioid cells and the myofibroblastic nature of the spindle tumor cells. We think the present tumor is a distinctive epithelioid fibrosarcoma with the combined features of SEFS and LGFMS/HSCT, suggesting their intimate relationship.

Adult↗
PubMed1997

Hydrops fetalis and fibrosarcoma: case report of an uncommon association.

UNLABELLED: Fetal hydrops associated with neonatal tumours is an uncommon occurrence. The diagnosis can be established prenatally by ultrasound examination. The treatment of choice is surgery which may be curative. We report the case of a male born at 32 weeks gestation who presented with severe hydrops fetalis and a thoracic mass. The child could not be operated upon because of rapid clinical deterioration. The autopsy findings confirmed the diagnosis of congenital fibrosarcoma. This is, to our knowledge, the first case of hydrops fetalis associated with fibrosarcoma. CONCLUSION: The association of hydrops fetalis and fibrosarcoma is an exceptional observation but can be added to the long list of differential diagnoses of non-immune hydrops.

Fatal Outcome↗
PubMed2005

Focal adhesion kinase is activated in invading fibrosarcoma cells and regulates metastasis.

Focal adhesion kinase (FAK) is a nonreceptor tyrosine kinase that is overexpressed in several human cancers, and induces survival, proliferation and motility of cells in culture. Phosphorylation of FAK has been studied extensively in vitro, but little is known about its regulation during tumor invasion in vivo. In the current study, green fluorescent protein (GFP) was expressed stably in an invasive murine fibrosarcoma cell line for the purpose of discrimination between tumor and normal cells. Under fluorescence microscopy, the tumor was highly fluorescent, and the margin between the tumor and normal tissue was clearly demarcated. Using this invasion model, we showed localization of pY397-FAK expression in the infiltrative edge of tumors. We reproduced local invasion in vivo using a tumor tissue culture method in a three dimensional collagen gel. Phosphorylation of FAK is also upregulated in invading fibrosarcoma cells under in vitro conditions. Expression of the FAK C-terminal domain termed FRNK (FAK-related non-kinase) in 2,472 cells decreased FAK phosphorylation without changing total FAK levels. FRNK inhibited the motility of 2,472 cells, and reduced invasion in vitro. Although FRNK did not affect cell growth, it inhibited experimental metastases in syngenic mice. These results demonstrate that the phosphorylation of FAK might be specifically upregulated in invading fibrosarcoma cells and regulate their invasion and metastasis.

Animals↗
PubMed1995

Congenital fibrosarcoma masquerading as congenital hemangioma: report of two cases.

The authors report on two infants who had large congenital fibrosarcomas that initially were believed to be hemangiomas. Although hemangioma and congenital fibrosarcoma can have a similar presentation, their treatment is dissimilar. The authors review the anatomic findings, hematologic differences, and radiological clues that can help to differentiate congenital fibrosarcoma from congenital hemangioma.

Diagnosis, Differential↗
PubMed1987

Plasminogen activator inhibitors from placenta and fibrosarcoma cells are antigenically different as evaluated with monoclonal and polyclonal antibodies.

Plasminogen activator inhibitor (PAI) purified from human placenta was compared to PAI purified from conditioned cell culture fluid of the human fibrosarcoma cell line HT-1080. The two inhibitors had a similar mobility (Mr approximately 50,000) in sodium dodecyl sulphate polyacrylamide gel electrophoresis (SDS-PAGE). Purified placental inhibitor revealed 2 major and 1 minor Coomassie blue stainable bands, while the fibrosarcoma inhibitor appeared as one band. By immunoblotting analysis both monoclonal and polyclonal antibodies against each of the inhibitors showed reaction with the inhibitor against which they were raised, but not cross reaction with the other inhibitor. Similar results were obtained, when antibody binding was tested by ELISA with the inhibitors coated on the solid phase. HPLC fingerprint patterns of cyanogen bromide fragments of the two inhibitors were different. The inhibitory activity of the placental PAI was decreased by a factor of 3 after incubation with SDS, while that of the fibrosarcoma PAI was increased by a factor of 30. It is concluded that the two inhibitors show no detectable common antigenic determinants and most likely are products of different genes.

Antibodies↗
PubMed1985

The nature of immunity to Snyder-Theilen fibrosarcoma virus induced tumors in cats.

Snyder-Theilen fibrosarcoma virus (ST-FeSV) induced tumors evoked a vigorous immune response in adolescent cats. The response was characterized histologically by a lymphoid and histiocytic cell infiltrate beginning around the 9th day post inoculation. Hyperemia edema, hemorrhage, and necrosis of the tumors occurred shortly thereafter. Gross regression of the tumors commenced around the 15th day. Viable fibrosarcoma cells could be recovered as almost pure cultures from tumors biopsied on the 9th day. Biopsies taken between days 9 and 15 contained progressively fewer tumor cells and increasing numbers of lymphoid cells, histiocytes, giant cells, and normal fibroblasts. Tumor cells in such mixed cultures did not replicate as fast as normal and died out within 7 to 14 days. Viable tumor cells were not recovered from biopsies taken after day 15. Fibrosarcoma regression was associated with the appearance of tumor cell specific cytotoxic lymphocytes and antibodies in the blood. Cell mediated immunity, as determined by a chromium release assay, consisted of both antibody dependent and independent mechanisms. Fluorescent and complement dependent cytolytic antibodies were detected in the blood at the same time as cytotoxic lymphocytes, but persisted after regression. In a preliminary experiment, serum from tumor regressor cats was injected into susceptible kittens, and the kittens were then challenged with ST-FeSV transformed fibroblasts or whole FeSV. Immune serum did not prevent the appearance of initial growth of tumors, but did slow their subsequent growth and increased the rate of regression. Immune serum had a much more dramatic inhibitory effect on the accompanying retrovirus infection.

Animals↗
PubMed1993

Consistent numerical chromosome aberrations in congenital fibrosarcoma.

Cytogenetic analysis of a congenital fibrosarcoma of the volar forearm from a 2.5-month-old boy revealed a mosaic karyotype 46,XY/49,XY,+11,+17,+20. This pattern of specific trisomies provides additional support to the cytogenetic findings in five cases of congenital fibrosarcoma reported previously. Trisomy 11 appears to be characteristic of congenital fibrosarcoma with additional trisomies 8, 17, and 20 as common findings.

Chromosome Aberrations↗
PubMed1993

Diagnostic imagings for primary cardiac fibrosarcoma.

Primary tumors of the heart are rare; primary cardiac fibrosarcoma is even rarer. We report a patient with primary cardiac fibrosarcoma widespread metastases presenting with pulmonary metastases initially. The cardiac lesion was identified by bone-imaging localization on bone scan, by hypodense areas in the cardiac chambers of contrast computed tomography of the chest, and by protruding masses in ventricular cavities causing aortic valve outflow-tract obstruction by echocardiogram. At autopsy, a large tumor invaded the interventricular septum and both ventricular cavities of the heart (880 g in weight), and accounted for these imaging findings. While bone-agent localization in the heart does not differentiate malignant from benign conditions, computed tomography and echocardiography of the interatrial and interventricular septal, and right atrial and biventricular cavitary involvement may differentiate fibrosarcoma from myxoma.

Aged↗
PubMed1991

Combined effects of synthetic lipid A analogs and muramyl dipeptide on antitumor activity against Meth A fibrosarcoma in mice.

Combined effects of chemically synthesized lipid A analogs, the compound A-171 (acylglucosamine-4-phosphate with (R)-3-hydroxytetradecanoyl and (R)-3-hydroxytetradecanoyloxy]tetradecanoyl group at the C-2 and C-3 positions), or the compound A-172 (with (R)-3-hydroxytetradecanoyloxy]tetradecanoyl and (R)-3-tetradecanoyloxytetradecanoyl group at the C-2 and C-3 positions), and muramyl dipeptide (MDP) on antitumor activity against Meth A fibrosarcoma, were examined. Meth A fibrosarcoma cells (5 X 10(5)) were inoculated intradermally into BALB/c mice on day 0, compound A-172 and/or MDP were administered intravenously (i.v.) on day 7. Although the antitumor activity by single i.v. injection of A-172 (50 micrograms/mouse) with MDP (10 micrograms) was weaker than that of 50 micrograms of synthetic lipid A analogs (506), or 10 micrograms of bacterial lipopolysaccharide (LPS) with MDP, A-172 alone and with MDP exhibited tumor inhibition rates of 49.0 and 70.6%, respectively. When A-171 (50 micrograms) with MDP (10 micrograms) was administered i.v. twice (days 7 and 10) into mice inoculated Meth A fibrosarcoma, two of five mice caused complete tumor regression. Furthermore, L929 cell lysis by the combination of A-171, A-172 with MDP was higher than that by the analogs or MDP alone, suggesting that the lipid A analogs of monosaccharide type as well as LPS are able to enhance the production of tumor necrosis factor in the presence of MDP.

Acetylmuramyl-Alanyl-Isoglutamine↗
PubMed1985

Activation of K-ras and oncogenes other than ras family in rat fibrosarcomas induced by 1,8-dinitropyrene.

Oncogenes of fibrosarcomas of rats, induced by subcutaneous injection of 1,8-dinitropyrene (1,8-DNP), were examined by NIH 3T3 cell transfection assay and Southern blot analysis. Transformants containing rat specific repetitive sequences were obtained with DNAs of 4 fibrosarcomas, 1,8-DNP1, 1,8-DNP2, 1,8-DNP3 and 1,8-DNP7. A transformant, 1,8-DNP2-2, induced by DNA of a fibrosarcoma, 1,8-DNP2, and 7 secondary transformants derived from it contained rat K-ras sequences. Another transformant, 1,8-DNP2-1, induced by the same sarcoma did not have a ras family oncogene. This indicates that the sarcoma, 1,8-DNP2, has at least 2 transforming genes. The transforming genes of 6 other transformants derived from 3 sarcomas did not contain ras family or neu transforming genes.

Animals↗
PubMed1996

Role of VLA-integrin receptor in invasion and metastasis of human fibrosarcoma cells.

Anti-invasive and anti-metastatic effects of anti-integrin antibodies (against VLA-alpha 2, alpha 4, beta 1) were examined on human fibrosarcoma cells using in vitro invasion assay in a reconstituted basement membrane (Matrigel) and experimental metastatic assay in a chick embryo. The effects of anti-integrin antibodies were compared with those of RGD-containing peptides (GRGDS), which have been known as effective inhibitors of tumor cell metastasis. Although slight differences in effective concentration among antibodies were observed, invasion and metastasis were significantly inhibited by anti-integrin antibodies. The results also showed partial inhibitory effect of GRGDS on the invasion and metastasis of human fibrosarcoma cells. These results indicate that integrin receptors mediating cell-cell/cell-extracellular matrix components interactions play a key role in the invasion and metastasis of human fibrosarcoma cells.

Animals↗
PubMed2006

Blood flow dependence of the intratumoral distribution of peripheral benzodiazepine receptor binding in intact mouse fibrosarcoma.

The intratumoral distribution of [(11)C]AC-5216 binding, a novel peripheral benzodiazepine receptor (PBR) ligand, was examined by autoradiography both in vitro and in vivo using a murine fibrosarcoma model. The regional distribution of [(11)C]AC-5216 in a tumor in vivo was significantly heterogeneous; the uptake of [(11)C]AC-5216 was comparatively higher in the outer rim of the tumor and was lower in the central area. In contrast, the images obtained following the injection of [(11)C]AC-5216 with a large amount of nonlabeled PK11195 showed a relatively homogeneous distribution, suggesting that [(11)C]AC-5216 uptake represented specific binding to PBRs. In vitro autoradiograms of [(11)C]AC-5216 binding were also obtained using the section of the fibrosarcoma that was the same as that used to examine in vivo binding. In vitro autoradiographic binding images showed homogeneous distribution, and significant discrepancies of the intratumoral distribution of [(11)C]AC-5216 were observed between in vivo and in vitro images. The in vivo images of [(11)C]AC-5216 uptake, compared with those of [(14)C]iodoantipyrine uptake, obtained by dual autoradiography to evaluate the influence of blood flow revealed the similar intratumoral distributions of both tracers. These results indicate that the delivery process from the plasma to the tumor might be the rate-limiting step for the intratumoral distribution of PBR binding in vivo in a fibrosarcoma model.

Animals↗
PubMed2002

Thymosin-beta4 regulates motility and metastasis of malignant mouse fibrosarcoma cells.

We identified a thymosin-beta4 gene overexpression in malignant mouse fibrosarcoma cells (QRsP-30) that were derived from clonal weakly tumorigenic and nonmetastatic QR-32 cells by using a differential display method. Thymosin-beta4 is known as a 4.9-kd polypeptide that interacts with G-actin and functions as a major actin-sequestering protein in cells. All of the six malignant fibrosarcoma cell lines that have been independently converted from QR-32 cells expressed high levels of thymosin-beta4 mRNA and its expression in tumor cells was correlated with tumorigenicity and metastatic potential. Up-regulation of thymosin-beta4 in QR-32 cells (32-S) transfected with sense thymosin-beta4 cDNA converted the cells to develop tumors and formed numerous lung metastases in syngeneic C57BL/6 mice. In contrast, antisense thymosin-beta4 cDNA-transfected QRsP-30 (30-AS) cells reduced thymosin-beta4 expression, and significantly lost tumor formation and metastases to distant organs. Vector-alone transfected cells (32-V or 30-V cells) behaved like their parental cells. We observed that tumor cell motility, cell shape, and F-actin organization is regulated in proportion to the level of thymosin-beta4 expression. These findings indicate that thymosin-beta4 molecule regulates fibrosarcoma cell tumorigenicity and metastasis through actin-based cytoskeletal organization.

Animals↗
PubMed1980

Bradykinin-stimulated release of arachidonate from phosphatidyl inositol in mouse fibrosarcoma cells.

We recently proposed a new pathway by which arachidonate is released from platelet phosphatidyl inositol after stimulation by either thrombin or calcium ionophore A23187. The initial step in arachidonate liberation involves hydrolysis of phosphatidyl inositol to form 1,2-diacyglycerol which is subsequently hydrolyzed by a diacyglycerol lipase to liberate arachidonate for the prostaglandin and lipoxygenase pathways. Whether this pathway is unique to platelets or accounts for arachidonate release from other tissues has not been previously studied. Thus we have now investigated arachidonate metabolism in mouse fibrosarcoma cells (HSDM1C1) grown in culture. These cells contain approximately 7.6% of their total phospholipid as phosphatidyl inositol in the resting state (range 6.5-8.3%). When bradykinin (12 microM) is added to the fibrosarcoma cells, there is a rapid depletion of membrane phosphatidyl inositol reaching 62 +/- 8% S.D. of baseline values by 15 seconds, falling to 36 +/- 6% by 15 minutes. The drop in membrane phosphatidyl inositol is accompanied by release of arachidonate and PGE2 into the culture medium. The time course of phosphatidyl inositol breakdown and PGE2 formation supports the idea that phosphatidyl inositol breakdown provides he arachidonate for prostaglandin synthesis in mouse fibrosarcoma cells. Crude extracts of HSDM1C1 cells contained sufficient phosphatidyl inositol-specific phospholipase C activity and diacylglycerol lipase activity to account for arachidonate release in these cells.

Arachidonic Acids↗
PubMed1998

Requirement of the CD8+ or CD4+ T lymphocyte subsets for the rejection of lymphoma and fibrosarcoma grafts studied in gene knockout hosts.

Rejections of the retrovirus induced lymphomas (ALC and RBL-5) and the methylcholanthrene (MCA) induced fibrosarcoma (MC57X) grafts were tested in syngeneic CD8 and CD4 single and double knockout C57BL/6 mice. The results with the lymphomas showed that the CD8+ T cell deficiency prevented the development of rejection response induced by immunization. Deficiency of the CD4+ T subset abrogated also the rejection of ALC. Immunity against the fibrosarcoma cells developed in both type of single knockout mice, but not in the ones which lacked both CD4+ and CD8+ T cells. Thus CD8+ T cells were required for rejection of the lymphoma cells, while the CD4+ T cells only mediated a weak response. In absence of CD8+ T cells, CD4+ T cells were sufficient to reject the fibrosarcoma cells.

Animals↗