SEARCH · PubMed Health

Results for “Fibrosarcoma”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

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

At least 37 records · Page 2Linked to original sources

PubMed2006

The apparent positive cooperativity of in vivo [3H]PK-11195 binding in mouse fibrosarcoma.

To evaluate the binding properties of peripheral benzodiazepine receptor (PBR) in mouse fibrosarcoma, [(3)H]PK-11195 binding, in vitro and in vivo, was investigated using either tissue dissection or autoradiographic method. The binding characteristics in fibrosarcoma were compared with those in the kidney. The results of an in vitro saturation study revealed that the maximal numbers of PBR binding sites (B(max)) in fibrosarcoma and in the kidney were almost the same (kidney: 5.2 pmol/mg protein; fibrosarcoma: 5.0 pmol/mg protein). On the other hand, the binding affinity (K(d)) in fibrosarcoma was lower than that in the kidney (kidney: 0.45 nM; fibrosarcoma: 1.34 nM). It is noteworthy that the in vivo binding of [(3)H]PK-11195 in fibrosarcoma increased with increasing doses of [(3)H]PK-11195 (in the dose range of 0.03-1 mg/kg), whereas that in the kidney decreased with competitive inhibition. The apparent positive cooperativity of [(3)H]PK-11195 binding in fibrosarcoma was only observed under in vivo conditions and might be possibly related to the incoordination of PBR subunits.

Animals↗

PubMed1996

Use of immunohistochemistry and polymerase chain reaction for detection of oncornaviruses in formalin-fixed, paraffin-embedded fibrosarcomas from cats.

OBJECTIVE: To determine whether there was intralesional infection or expression of FeLV or feline sarcoma virus in suspected vaccine-associated fibrosarcomas in cats. DESIGN: Prospective case series. SAMPLE POPULATION: 130 suspected vaccine-associated fibrosarcomas from cats and 1 multicentric fibrosarcoma from 1 cat. PROCEDURE: Excisional biopsy specimens were fixed in formalin and embedded in paraffin. Expression of FeLV antigen was assessed, using a polyclonal goat anti-FeLV glycoprotein 70 (gp 70) serum and an avidinbiotin immunoperoxidase staining technique. The FeLV genome was detected with a polymerase chain reaction (PCR), using primers targeted to a conserved sequence in the untranslated region of the long terminal repeat (LTR) of the FeLV. RESULTS: FeLV gp 70 and LTR sequence were detected in a multicentric fibrosarcoma. All 130 of the suspected vaccine-associated fibrosarcomas were FeLV gp 70 negative on the basis of immunohistochemical test results: 100 fibrosarcomas also were examined by use of PCR and were negative for FeLV LTR region. CLINICAL IMPLICATIONS: Exogenous retroviruses, FeLV, and feline sarcoma virus were not detected in these suspected vaccine-associated fibrosarcomas, using immunohistochemistry and PCR. Additional testing will be required to determine the nature of genomic alterations that are involved in the oncogenesis of vaccine-associated fibrosarcomas in cats.

Animals↗

PubMed1986

Effects of verapamil and alcohol on blood flow, melphalan uptake and cytotoxicity, in murine fibrosarcomas and human melanoma xenografts.

Verapamil had previously been shown to increase cellular melphalan uptake and cytotoxicity in fibrosarcomas, and increased the area under the blood concentration versus time curve (AUC) for melphalan in CBA mice. Verapamil (10 mg kg-1 i.p.) had no effect on the fractional distribution of cardiac output (FDCO), measured with 86Rb-rubidium chloride, to subcutaneous fibrosarcomas. 14C-Melphalan uptake by FS13 fibrosarcomas was increased 60 min after verapamil (10 mg kg-1 i.p.), but not after lower doses which did not affect the AUC. Flunarizine (5 mg kg-1 i.p.) also had no effect on FDCO to FS13 fibrosarcomas, and tended to increase 14C-melphalan content of blood and the fibrosarcomas and to promote growth delay by melphalan. Alcohol increased FDCO to FS13 fibrosarcomas, maximally at a 1:20 dilution in saline, but had no effect on 14C-melphalan uptake or growth delay. Thus, melphalan cytotoxicity correlated with tumour melphalan uptake, and both followed changes in the AUC for melphalan but not changes in FDCO. In these murine fibrosarcomas melphalan uptake and cytotoxicity were not limited by blood flow. In subcutaneous human melanoma HX46 xenografts, verapamil had no effect on the FDCO, nor on 14C-melphalan uptake, and did not affect blood 14C-melphalan levels, suggesting absence of effects on the AUC and on cellular uptake. Alcohol did not increase the FDCO to HX46 xenografts, providing evidence for a different vascular supply.

Animals↗

PubMed1994

Fibrosarcoma in infants and children. Application of new techniques.

Fibrosarcomas occurring in infants and young children are intriguing tumors. Although biologically more benign than their counterparts occurring in old patients, they are histologically similar. Microscopically, they fit in one end of a spectrum of fibrous proliferations occurring in the pediatric population. Prompted by recent karyotypic reports of nonrandom gains of chromosomes 8, 11, 17, and 20 in infantile fibrosarcomas, we retrospectively analyzed 12 infantile fibrosarcomas utilizing fluorescence in-situ hybridization (FISH) with chromosome 8-, 11-, 17-, and 20-specific probes. Parallel studies were performed on fibrosarcomas occurring in older children and young adults and also on cellular fibromatoses, myofibromatoses, and fibromatoses. Gains of chromosomes 8, 11, 17, and 20 (in various combinations) were observed in 11 of 12 fibrosarcomas occurring in infants < 2 years of age. Extra copies of chromosomes 17 and 20 were observed in a fibrosarcoma occurring in a 5-year-old child but no abnormalities were detected by FISH in four additional fibrosarcomas occurring in patients aged 6-17 years. One of three cellular fibromatoses was characterized by extra copies of chromosome 8, 11, 17, and 20. Similar findings were not observed in any of the noncellular fibromatoses or in myofibromatoses.

Adolescent↗

PubMed2006

Immune phenomena involved in the in vivo regression of fibrosarcoma cells expressing cell-associated IL-1alpha.

Constitutive expression of cell-associated, but not secreted, interleukin-1alpha (IL-1alpha) by oncogene-transformed fibrosarcoma cells induced regressing tumors in mice, a phenomenon that was abrogated by the IL-1 inhibitor, the IL-1 receptor antagonist (IL-1Ra). On the contrary, non-IL-1alpha-expressing tumor cells induce progressive tumors in mice. In vivo and ex vivo experiments have shown that regression of IL-1alpha-positive fibrosarcoma cells depends on CD8(+) T cells, which can also be activated in CD4(+) T cell-depleted mice, with some contribution of natural killer cells. In spleens of mice bearing the non-IL-1alpha-expressing fibrosarcoma cells, some early and transient manifestations of antitumor-specific immunity, such as activation of specific proliferating T cells, are evident; however, no development of cytolytic T lymphocytes or other antitumor protective cells could be detected. In spleens of mice bearing the non-IL-1alpha-expressing fibrosarcoma cells, the development of early tumor-mediated suppression was observed, and in spleens of mice injected with IL-1alpha-positive fibrosarcoma cells, protective immunity developed in parallel to tumor regression. Treatment of mice bearing violent fibrosarcoma tumors with syngeneic-inactivated, IL-1alpha-positive fibrosarcoma cells, at a critical interval after injection of the malignant cells (Days 5-12), induced tumor regression, possibly by potentiating and amplifying transient antitumor cell immune responses or by ablation of tumor-mediated suppression. Membrane-associated IL-1alpha may thus serve as an adhesion molecule, which allows efficient cell-to-cell interactions between the malignant and immune effector cells that bear IL-1Rs and function as a focused cytokine with adjuvant activities at nontoxic, low levels of expression. Our results also point to the potential of using antitumor immunotherapeutic approaches using cell-associated IL-1alpha.

Animals↗

PubMed2004

Sp1 regulates expression of MET, and ribozyme-induced down-regulation of MET in fibrosarcoma-derived human cells reduces or eliminates their tumorigenicity.

Changes in expression of hepatocyte growth factor (HGF) and its receptor, MET, are associated with formation and malignant progression of human tumors. In the present study, 10 of 11 human fibrosarcoma cell lines tested expressed significantly higher levels of MET than were found in a series of normal human fibroblast lines. Still more significant, MET was constitutively phosphorylated in all 11 fibrosarcoma lines, whereas the normal fibroblasts exhibited very low levels of the phosphorylated form. All the cell lines expressed HGF mRNA. To determine the role of MET and/or HGF in tumorigenesis, a fibrosarcoma line expressing high levels of MET protein and low levels of HGF/NK2 mRNA was stably transfected with a hammerhead ribozyme targeting MET. In addition, a fibrosarcoma line expressing high levels of both MET protein and HGF/NK2 mRNA was transfected with a ribozyme targeting MET, or with a ribozyme targeting MET and another targeting HGF. The transfectant cell lines no longer formed tumors, or did so at a greatly reduced frequency and/or longer latency. Because Sp1 is a transcription factor for MET, we assayed the cell lines for their level of Sp1 protein. Sp1 was markedly overexpressed in 7 of the 11 fibrosarcoma lines compared to normal fibroblast lines. Deletion analysis and site-directed mutagenesis of the MET promoter revealed that tandem Sp1 sites in the proximal promoter are critical for transcription of MET. Increased expression of Sp1 in a normal human fibroblast line containing a MET promoter-luciferase construct resulted in a dose-dependent increase in luciferase. Conversely, inhibition of Sp1 binding to DNA in a fibrosarcoma cell line, using an Sp1 decoy, dramatically reduced MET expression. Taken together, these results indicate that in human fibrosarcoma cells, high levels of the phosphorylated form of MET are required for tumor formation and that Sp1 can function to control the level of MET.

Animals↗

PubMed1986

In vitro and in vivo interaction between murine fibrosarcoma cells and natural killer cells.

Murine fibrosarcoma cells were examined for sensitivity to killing by natural killer (NK) and natural cytotoxic lymphocytes from mouse spleens. These tumor cell lines were sensitive to killing by effector cells which were nonadherent to plastic or nylon wool, Thy-1 negative, asialo-GM1 negative, and present in the spleens of beige mice, nude mice, and A/J mice, as well as in the spleens of normal syngeneic and allogeneic control mice. This indicates that the cytotoxic effects were due to natural cytotoxic lymphocytes rather than to NK lymphocytes, T-cells, or macrophages. Although the fibrosarcoma cells were not killed in vitro by endogenous NK cells, these tumor cells were able to "cold target" compete for Yac-1 (an NK-sensitive target) killing and to bind to asialo-GM1-positive, nonadherent spleen lymphocytes in a target cell binding assay. This suggests that the fibrosarcoma cells were recognized by NK cells. In addition, these cell lines were killed in a 4-h NK cytotoxicity assay by polyinosinic-polycytidylic acid-activated effector lymphocytes. The interaction between NK cells and the murine fibrosarcoma cells may have in vivo significance. When syngeneic mice were treated with anti-asialo-GM1 serum to eliminate NK activity and then given i.v. injections of the fibrosarcoma cells, many more lung tumors developed than in control animals. The structural basis for the recognition of the murine fibrosarcoma cells by the NK effector cells is not known. However, laminin may be involved. When the fibrosarcoma cells, which have receptors for the laminin molecule, were preincubated with laminin, they were reduced in their ability to compete for the killing of Yac-1 cells by the NK effectors and had reduced capacity to bind to NK cells in a target cell binding assay.

Animals↗

PubMed1988

Differential immunoreactivity and Ca2+-dependent degradation of vimentin in human fibroblasts and fibrosarcoma cells.

Immunostaining of normal human fibroblasts with a monoclonal antibody (MAb) (V22AC12) revealed typical cytoplasmic arrays of vimentin filaments in both mitotic and interphase cells. In human A8387 fibrosarcoma cells and SV40-virus-transformed human fibroblasts, the same antibody showed positivity only in mitotic cells and in interphase cells only after treatment of the fixed cells with alkaline phosphatase. Upon immunoblotting with the MAb, an Mr 57,000 vimentin polypeptide was seen in normal fibroblasts. In fibrosarcoma cells the same polypeptide was revealed by this antibody only after treatment with alkaline phosphatase. The Mr 57,000 vimentin polypeptide was a major cytoskeletal protein in both fibroblasts and fibrosarcoma cells. Inclusion of Ca2+ into the cytoskeleton extraction medium brought about a somewhat increased degradation of vimentin in fibroblasts. In fibrosarcoma cells, such treatment caused a quantitative disappearance of the Mr 57,000 protein with a concomitant appearance of 3 distinct, low-molecular-weight degradation products in the detergent-soluble fraction. Another Ca2+-induced change in the polypeptide profile of fibrosarcoma cells was the disappearance of the Mr 240,000 non-erythroid alpha-spectrin and the concomitant appearance of a prominent Mr 140,000 degradation product. Inclusion of proteolysis inhibitors in the Ca2+-supplemented extraction medium inhibited degradation of both vimentin and alpha-spectrin polypeptides. The results suggest differences in the composition of the cytoskeletons of normal fibroblasts and fibrosarcoma cells, manifested in the differential Ca2+-susceptibility of vimentin and non-erythroid alpha-spectrin. Results with MAb V22AC12 suggest that differential phosphorylation of vimentin could account for at least part of this difference.

Antibodies, Monoclonal↗

PubMed2001

Fibrosarcoma in pediatric patients: results of the Italian Cooperative Group studies (1979-1995).

BACKGROUND AND OBJECTIVES: Fibrosarcoma is a rare soft tissue sarcoma (STS) that has two peaks of incidence in pediatric patients: one in infants and young children (infantile fibrosarcoma), another in older children ("adult type" fibrosarcoma). The purpose of this study was to describe the clinical features and the treatment results in patients affected by fibrosarcoma enrolled in two consecutive studies run by the STS-Italian Cooperative Group (ICG) between 1979 and 1995. PATIENTS AND METHODS: Twenty-five evaluable patients were grouped according the intergroup rhabdomyosarcoma staging (IRS) system: 12 Gr I, 5 Gr II, 8 Gr III. The cut-off point between the two forms was considered the age of 2 years: 14 patients were affected by infantile and 11 by adult type of fibrosarcoma. The therapeutic guidelines were not strict and not different for the two forms: patients with initial macroscopic excision (Gr I-II) were given IVA or VAC; Gr III had VAC or VAIA and subsequent excision, if feasible. Radiation therapy (RT) was delivered in patients > 3 years with microscopic (42 Gy) and macroscopic (54 Gy) residuals. RESULTS: Thirteen patients are alive without evidence of disease: 10 in first complete remission (CR), 7 Gr I, 1 Gr II, 2 Gr III, 3 in second CR after local relapse (LR) (2 Gr I, 1 Gr II). Two Gr I patients are alive with metastatic relapse. Nine patients died: six of progressive disease (PD) (three Gr II, three Gr III), two because of a second tumor (one Gr I, one Gr III) and one because of other causes (Gr III). One Gr III patient was lost at follow up, 2 years from diagnosis. The 10 years overall survival (OS) is 67.4% and the progression-free survival (PFS) is 52.2%. The OS for patients < 2 years is 78.6% (11 of 14), versus 51% for patients > 2 years (5 of 11). CONCLUSIONS: The complete excision at diagnosis was the treatment of choice and was related to the best outcome. Microscopical residuals were difficult to treat with chemo-radiotherapy in both forms of fibrosarcoma. Neoadjuvant chemotherapy (CT) obtained a partial remission (PR) only in three of eight cases, while no conclusions concerning the efficacy of CT for infantile forms are possible. Patients < 2 years had a better outcome than the older ones: most of them had a tumor on extremities which was excised at diagnosis.

Adolescent↗

PubMed2001

Expression of COL1A1-PDGFB fusion transcripts in superficial adult fibrosarcoma suggests a close relationship to dermatofibrosarcoma protuberans.

The diagnosis of fibrosarcoma has become relatively rare since the recognition and definition of certain adult spindle-cell sarcomas, such as monophasic synovial sarcoma, malignant peripheral nerve sheath tumour (MPNST), and malignant fibrous histiocytoma (MFH). Although most adult fibrosarcomas occur within intra- or inter-muscular fibrous tissues, some originate from superficial soft tissues (superficially located adult fibrosarcomas) (SAFs). Recently, the COL1A1-PDGFB chimeric gene resulting from a reciprocal translocation, t(17;22), and/or a supernumerary ring chromosome, r(17;22), has been identified, not only in conventional dermatofibrosarcoma protuberans (DFSP) but also in areas of DFSP with progression to fibrosarcoma (so-called fibrosarcomatous transformation) (FS-DFSP). Since many SAFs are clinically and histologically similar to DFSP or FS-DFSP, this study postulated that the two groups may be interrelated histogenetically. To test this hypothesis, a reverse transcription-polymerase chain reaction (RT-PCR) assay was conducted to determine whether COL1A1-PDGFB fusion transcripts could be detected in six cases of SAF, using archival formalin-fixed, paraffin-embedded tissues. COL1A1-PDGFB fusion transcripts were detected in four of six SAFs, whereas no such fusion transcripts could be amplified in five deep-seated fibrosarcomas, eight congenital/infantile fibrosarcomas or 28 other spindle-cell tumours and tumour-like lesions. These results show that at least some cases of SAF are genetically similar to DFSP and FS-DFSP, suggesting that some SAFs originate from DFSP or involve similar pathogenetic mechanisms.

Adult↗

PubMed1993

Purification and characterization of collagens from rat fibrosarcoma induced by 3-methylcholanthrene.

The distribution of various collagen types was studied in rat fibrosarcoma. Collagens extracted from fibrosarcoma tissue were characterized by the criteria of solubility in NaCl, SDS-PAGE, ion exchange chromatography, CNBr peptide mapping and amino acid analysis. Fibrosarcoma was found to produce excess amount of type V, type I trimer and type III collagens; comparatively, type I collagen and total collagen content were noticed to decrease in fibrosarcoma. We observe that the increase in type V collagen content in fibrosarcoma might be due to the enhanced transcription of type V collagen gene. Increased type I trimer collagen in fibrosarcoma might be attributed to the differential expression of alpha 1(I) and alpha 2(I) gene and might also be due to the expression of a different gene for type I trimer collagen.

Animals↗

PubMed1985

Immunotherapeutic studies of different clonal lines of herpesvirus-induced fibrosarcoma in a syngeneic rat.

Transformation of White Buffalo rat embryonic cells by dye-light-inactivated herpesvirus type 2 resulted in the development of two clones of transformed cells (G2 and rat fibrosarcoma) with significantly different tumorigenic capabilities. The G2 cell line was initially nontumorigenic, while the rat fibrosarcoma line was very highly tumorigenic in rats. These significant differences in transformed cell clones from the same initial culture offered an opportunity to study aspects of the immunobiology of oncogenicity. The development of fibrosarcomas in immunoincompetent nude mice with the same early passages of the G2 cell line which were nontumorigenic in the immunocompetent rat suggested that immunologic resistance developed more effectively in the competent host against the G2 line than against rat fibrosarcoma cells. Syngeneic rats which were first exposed to the early passage nontumorigenic G2 cells were completely protected against tumor development by the rat fibrosarcoma cell lines. In subsequent in vitro passages of the G2 cell line, it lost its ability to protect against rat fibrosarcoma challenge and gradually became oncogenic in rats. Modification of antigenic exposure, accomplished by treating the G2 cells with cholesteryl hemisuccinate, resulted in an increase in the protection by these cells and a delay in tumor development.

Animals↗

PubMed1997

Fibrosarcoma versus cellular fibroma of the ovary: a comparative study of their proliferative activity and chromosome aberrations using MIB-1 immunostaining, DNA flow cytometry, and fluorescence in situ hybridization.

We retrospectively analyzed the proliferative activity and the centromeric copy number of chromosomes 8, 12, and 17 in three cases of fibrosarcoma and eight cases of cellular fibroma of the ovary using MIB-1 immunostaining, DNA flow cytometry, and fluorescence in situ hybridization (FISH) on paraffin-embedded tissue specimens. In our study, both the MIB-1 labeling index (LI) and the proliferative index (% of cells in S + G2 + M phase) in fibrosarcomas were higher than those in cellular fibromas. The FISH analysis demonstrated the sole abnormality of a gain of trisomy 12 cells in all eight cases of cellular fibroma. Both a gain of trisomy 12 cells and a gain of tetrasomy 12 cells were observed in one case of fibrosarcoma. A gain of trisomy 8 cells was observed in all two fibrosarcomas in which signals were detected. By contrast, neither a gain of trisomy 8 cells nor a gain of tetrasomy 12 cells was observed in any of the eight cases of cellular fibroma. Chromosome 17 showed disomy in all eleven cases. On the basis of these findings, a gain of trisomy 8 cells is therefore considered to be an adequately effective marker to distinguish between cellular fibroma and fibrosarcoma of the ovary, and it may also be related to the proliferative activity of fibrosarcoma of the ovary.

Adolescent↗

PubMed1979

Infantile and adult fibrosarcomas of the soft tissues.

Histologic sections of 68 soft-tissue sarcomas initially diagnosed as fibrosarcoma were reviewed, and 36 were excluded because of revised diagnosis. The tumors from the remaining 32 patients were analyzed clinicopathologically, and were classifed into two types; the adult type (22 cases) and the infantile type (10 cases). The adult type fibrosarcoma occurred in adults aged 25 to 67 years and consisted of spindle-shaped fibroblastic cells which formed interlacing bundles accompanied by variable amounts of collagen or reticulin fibers. The infantile fibrosarcoma affected children below the age of seven years in this series and was characterized by proliferation of immature fibroblasts forming indistinct bundles, frequently exhibiting areas of an angiosarcoma-like pattern and cavernous blood vessels. The authors expressed the view that infantile fibrosarcoma should be separated from adult fibrosarcoma, because between these two types of fibrosarcoma there were marked differences in the histologic feature as well as in the age, sex and anatomical distributions.

Adult↗

PubMedDate not supplied

Congenital infantile fibrosarcoma of the thigh in a newborn.

Congenital/infantile fibrosarcoma occurs frequently in the first year of life and differs from fibrosarcoma in adulthood. The clinical course of congenital/infantile fibrosarcoma is more favorable and metastatic spread is rare. While adult fibrosarcomas are common in the thigh, congenital/infantile fibrosarcomas affect chiefly the distal portions of the extremities. Standard treatment is primarily wide surgical excision. Chemotherapy may be given as neoadjuvant or adjuvant treatment in order to avoid the morbidity associated with wide excision. In this case report we present our experience of a newborn affected by congenital/infantile fibrosarcoma of the left thigh.

Antineoplastic Combined Chemotherapy Protocols↗

PubMed2004

Antitumor effectiveness of different amounts of electrical charge in Ehrlich and fibrosarcoma Sa-37 tumors.

BACKGROUND: In vivo studies were conducted to quantify the effectiveness of low-level direct electric current for different amounts of electrical charge and the survival rate in fibrosarcoma Sa-37 and Ehrlich tumors, also the effect of direct electric in Ehrlich tumor was evaluate through the measurements of tumor volume and the peritumoral and tumoral findings. METHODS: BALB/c male mice, 7-8 week old and 20-22 g weight were used. Ehrlich and fibrosarcoma Sa-37 cell lines, growing in BALB/c mice. Solid and subcutaneous Ehrlich and fibrosarcoma Sa-37 tumors, located dorsolaterally in animals, were initiated by the inoculation of 5 x 10(6) and 1 x 10(5) viable tumor cells, respectively. For each type of tumor four groups (one control group and three treated groups) consisting of 10 mice randomly divided were formed. When the tumors reached approximately 0.5 cm3, four platinum electrodes were inserted into their bases. The electric charge delivered to the tumors was varied in the range of 5.5 to 110 C/cm3 for a constant time of 45 minutes. An additional experiment was performed in BALB/c male mice bearing Ehrlich tumor to examine from a histolological point of view the effects of direct electric current. A control group and a treated group with 77 C/cm3 (27.0 C in 0.35 cm3) and 10 mA for 45 min were formed. In this experiment when the tumor volumes reached 0.35 cm3, two anodes and two cathodes were inserted into the base perpendicular to the tumor long axis. RESULTS: Significant tumor growth delay and survival rate were achieved after electrotherapy and both were dependent on direct electric current intensity, being more marked in fibrosarcoma Sa-37 tumor. Complete regressions for fibrosarcoma Sa-37 and Ehrlich tumors were observed for electrical charges of 80 and 92 C/cm3, respectively. Histopathological and peritumoral findings in Ehrlich tumor revealed in the treated group marked tumor necrosis, vascular congestion, peritumoral neutrophil infiltration, an acute inflammatory response, and a moderate peritumoral monocyte infiltration. The morphologic pattern of necrotic cell mass after direct electric current treatment is the coagulative necrosis. These findings were not observed in any of the untreated tumors. CONCLUSION: The data presented indicate that electrotherapy with low-level DEC is feasible and effective in the treatment of the Ehrlich and fibrosarcoma Sa-37 tumors. Our results demonstrate that the sensitivity of these tumors to direct electric current and survival rates of the mice depended on both the amount of electrical charge and the type of tumor. Also the complete regression of each type of tumor is obtained for a threshold amount of electrical charge.

Animals↗

PubMed2001

Cytoskeletal-induced alterations in the adhesion of HT-1080 fibrosarcoma cells to extracellular matrix.

We have investigated the adhesion of the human fibrosarcoma cell line, HT-1080, transfected with glial fibrillary acidic protein (GFAP) to a variety of extracellular matrix macromolecules (ECM) including collagen type IV, laminin, and fibronectin. The GFAP-transfectants demonstrated altered adhesiveness to extracellular matrix substrates when compared to controls. GFAP-positive, heavy metal-induced fibrosarcoma cells were more adherent to plastic and collagen type IV than were the parental or uninduced cells. In contrast, GFAP-positive fibrosarcoma cells were less adherent to laminin- or fibronectin-coated dishes than controls. Time course adhesion studies over 9 days showed that the heavy metal-induced fibrosarcoma cells progressively became more adherent to collagen type IV and less adherent to laminin- or fibronectin-coated dishes than did uninduced cells. However, with the removal of heavy metal from the medium, the HT-1080 fibrosarcoma cells were restored to their original adhesive potential. By phase microscopy, uninduced and induced HT-1080 cells demonstrated different morphological features and remained viable in an anchorage-dependent fashion on collagen type IV as a substrate. By way of contrast, GFAP-induced HT-1080 cells were not particularly viable in monolayer culture and readily detached from laminin as a substrate. The expression of beta1 integrin in GFAP-positive fibrosarcoma cells was decreased following heavy metal induction by Western blot analyses. In contrast, the expression of alpha2 integrin was increased whereas alpha5 integrin was unchanged in HT-1080 cells following the induction of GFAP. Gelatin zymography showed that 72 kDa collagenase was less expressed in GFAP-induced clones than in controls. Our data suggest that the forced expression of the intermediate filament, GFAP, in HT-1080 cells may modulate cell adhesion to different ECM substrates through alterations in expression of integrins.

Blotting, Western↗

PubMed1990

[Ultrastructural study of fibrosarcoma].

Ultrastructure of 9 cases of fibrosarcoma was observed and compared with that of fibrous connective tissue of 4 human embryos and 9 cases of spindle cell sarcoma, including 3 each of leiomyosarcoma, neurofibrosarcoma and dermatofibrosarcoma protuberans. Ultrastructurally, fibrosarcoma consisted of well-differentiated fibroblast-like cells, poorly differentiated fibroblast-like cells (embryonic fibroblast-like cells), myofibroblast-like cells and primitive mesenchymal cells. It is suggested that fibrosarcoma may arise from primitive mesenchymal cells which are capable of differentiating into fibroblast and myofibroblast. There were two special cases of fibrosarcoma in this series. One was a congenital fibrosarcoma with ultrastructure resembling adult and the other was a sarcoma of myofibroblast. Diagnosis and differential diagnosis between fibrosarcoma and leiomyosarcoma, neurofibrosarcoma, dermatofibrosarcoma protuberans are discussed.

Adolescent↗