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At least 1,207 records · Page 67Linked to original sources
PubMed1989

[Ultrasonic tomography in assessing the efficacy of the combined treatment of fibrosarcoma].

Ultrasonic tomography was used in 40 patients with locally-advanced fibrosarcoma of soft tissues who had undergone polychemotherapy or radiation in combination with short-term (5-10 minutes) ultrasound or microwave treatment of physical therapy intensity (1-2 W/cm2) given as a modifier. These procedures were used prior to surgery in 24 cases and as the only treatment--in 16. Ultrasonic tomography was performed before start, in the middle and right after termination of therapy, and before surgery. Addition of short-term ultrasound and microwave treatment was followed by formation of dense fibrous capsule around the tumor which assured a longer (3-5 years) recurrence-free survival. Ultrasonic tomography allows to monitor formation of the capsule and is, therefore, useful for assessing treatment outcome, making prognosis and determining time and extent of surgery.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1989

[Neonatal pulmonary fibrosarcoma].

The authors report a case of pulmonary fibrosarcoma in a newborn. The respiratory distress imposed an urgent thoracotomy at the fifth hour of live. A lobectomy was performed. Three months later a relapse occurred. A second thoracotomy permitted an incomplete resection. The total involution was achieved after 6 months of chemotherapy. Actually no recidive is shown after 20 months of follow up. Its an exceptional case. A unique one was published in 1977.

Fibrosarcoma↗
PubMed1989

Surgical solution of femoral fibrosarcoma. Experience obtained by a 9-year follow-up.

Biopsy followed by tumour removal and replacement by autologous bone tumour at the distal end of the femur were performed. Histologically, the tumour proved to be benign. Three years later progression was observed and epiphyseodiaphyseal resection was made because of on excessive tumour. Histology revealed a fibrosarcoma. Consolidation was hindered by osteomyelitis and fracture, recovery could be achieved only by a series of operations. These histological and operative difficulties are documented and the importance of extremity-saving operations is discussed. Our patient has been free of complaints 9 years after epiphyseodiaphyseal reseaction.

Adult↗
PubMed1989

[A case of radiation-induced intracranial fibrosarcoma with repeated episodes of intratumoral hemorrhage].

A fibrosarcoma developed 10 years after radiotherapy for craniopharyngioma in a 19-year-old girl is reported. The mode of presentation in this patient was unique. She had repeated episodes of intracranial bleeding which mimicked hemorrhagic cerebral infarction, and there was also an extremely rapid regrowth of the tumor after each resection. Chemotherapy with ACNU, cisplatin and adriamycin was transiently effective in the stormy course of this patient. The occurrence of radiation induced intracranial tumor should be kept in mind in the follow up study of patients with benign brain tumors who have received radiation therapy.

Adult↗
PubMed1989

Primary intraosseous fibrosarcoma in a cat.

A primary intraosseous fibrosarcoma was diagnosed in a 1.5-year-old cat. Clinical signs included nonweight-bearing lameness of the right forelimb and signs of pain on palpation of the right elbow. Radiography of the right elbow revealed a well-circumscribed osteolytic lesion of the olecranon. The right fore-limb was amputated, and histologic examination revealed tumor invasion into local veins and metastasis to the axillary lymph nodes. The cat had no signs of tumor redevelopment or pulmonary metastatic disease one year after amputation.

Amputation, Surgical↗
PubMed1988

The immunobiology of metastatic processes: analysis of NK sensitivity and the metastatic potential of H-2 gene transfected fibrosarcoma cells.

The transformation of a potentially neoplastic cell into an autonomous highly malignant and metastatic tumor cell involves a multifactorial cascade of events. This will eventually lead not only to the emergence of a tumor cell with an unlimited potential of replication, but more important will contribute to its ability to ignore and evade homeostatic immune and nonimmune regulatory mechanisms. Specifically, those mechanisms which may restrict and direct its growth, dissemination, patterns of differentiation and interaction with the cellular and humoral factors comprising its environment. In the present studies we have investigated the contribution of three major factors which may be the cause or result of alterations at the level of the cell membrane: MHC encoded antigen expression, susceptibility to the cytolytic activity of NK cells and enhanced expression of the c-K-ras proto-oncogene, as to their development of the metastatic capacity of a malignant cell. To address these questions we used metastatic (IE7) and nonmetastatic (IC9) variants of the murine 3-methylcholanthrene-induced T-10 fibrosarcoma. Using this system, the following major conceptually important observations were made: (A) The restoration by transfection of the expression of membrane associated H-2K encoded glycoproteins abrogates the metastatic capacity of the highly metastatic tumor cell clone, IE7, irrespective of the degree of susceptibility to NK or c-K-ras oncogene expression.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Relationship between energy status, hypoxic cell fraction, and hyperthermic sensitivity in a murine fibrosarcoma.

The energy status, radiobiological hypoxic cell fraction, and hyperthermic sensitivity of a spontaneous murine fibrosarcoma, FSa-II, have been evaluated as a function of tumor size. Tumors were evaluated over the size range of 70 to 800 mm3. The concentration of the high-energy phosphate reservoir creatine phosphate progressively decreased by a factor of 5 with increasing tumor volume, and was matched by an increase in creatine. The concentration of ATP also decreased with increasing tumor size, although this decrease was substantially less pronounced. The sum of ATP, ADP, and AMP did not vary with tumor size, suggesting that the necrotic fraction remained constant. The decrease in energy status occurred in parallel with an increase in the size of the hypoxic cell fraction and with increasing thermal sensitivity. The results suggest that energy status may be an important modifier of hyperthermic sensitivity in vivo and reflect tissue oxygen concentration.

Adaptation, Physiological↗
PubMed1985

Cell surface antigens of chemically induced fibrosarcomas: detection by a monoclonal antibody of a tumor-restricted Mr 12,000 protein gag antigen encoded by a dual-tropic murine leukemia virus.

Fusion products of spleen cells of W/FuDp rats immunized with a methylcholanthrene-induced BALB/c sarcoma, CA-2, and mouse myeloma cells were screened in an attempt to identify a monoclonal antibody defining the individually distinct tumor-specific transplantation antigen of CA-2. A hybridoma, MP/69/04, was isolated which produces an IgG2a monoclonal antibody that recognized a tumor-restricted antigen of CA-2. In direct binding assay, MP/69/04 reacted only with 2 of 15 methylcholanthrene induced BALB/c sarcomas tested. Thymus, spleen, lymph nodes, bone marrow, brain, adult lung fibroblasts, newborn muscle fibroblasts and 3T3 cells were negative. Absorption tests revealed, however, expression of the MP/69/04 determinant on 8 of the 12 murine leukemia virus (MuLV) producer BALB/c sarcoma tested. The antigen was not detected on any of the three non-producer sarcomas tested nor on a wide range of normal tissues and cell lines. An N-dualtropic MuLV was isolated from CA-2, and cell lines susceptible to infection by this virus were shown to express the MP/69/04 epitope. By Western blotting, the MP/69/04 epitope was identified as being expressed on the MuLV structural protein with a molecular weight of 12,000, present in CA-2 cells and in the purified CA-2 MuLV. These results indicate the MP/69/04 antigen is not a unique tumor-specific transplantation antigen but is a gag product of a recombinant retrovirus which is expressed on the cell surface of many MuLV + methylcholanthrene-induced BALB/c fibrosarcomas.

Animals↗
PubMed1987

Inhibition of established rat fibrosarcoma growth by the glucose antagonist 2-deoxy-D-glucose.

Sarcoma cells exhibit higher rates of glycolysis than normal tissues and may be dependent on glucose utilization for growth. Accordingly, we tested the ability of the glucose antimetabolite 2-deoxy-D-glucose (2-DG) to inhibit the growth of an established methylcholanthrene-induced rat fibrosarcoma in three groups of F344 rats with increasing subcutaneous inoculations of tumor (2 X 10(6) cells, 1 X 10(7) cells, and 1 mm tumor fragments). Rats were randomized to receive 2-DG or saline solution at doses of 0.75 gm/kg, 1.5 gm/kg, or 1.75 gm/kg, beginning 3 days after tumor implantation and continuing for 10 days. Tumors were removed and weighed on day 14. We measured tissue [14C]-2-DG levels in tumor, brain, liver, and muscle after intraperitoneal injection of radiolabeled 2-DG. In these same tissues we determined the activity of glucose-6-phosphatase (G-6-Pase), an enzyme which dephosphorylates the intracellular glycolytic inhibitor 2-DG-6-phosphate, thus reversing the antitumor effect of 2-DG. All groups treated with 2-DG had a significant reduction in tumor weight of 50% to 70% when compared with saline solution-treated controls. Toxicity was substantial at the highest dose of 2-DG, but minimal toxicity was noted at intermediate and low doses. Tumor had the greatest uptake of [14C]-2-DG, with low levels of G-6-Pase leading to prolonged retention and highest tissue levels of radiolabeled 2-DG. Use of 2-DG inhibits established sarcoma growth because it is rapidly transported into tumors, cannot be metabolized after phosphorylation, and is dephosphorylated and released slowly from tumor cells. Rat sarcoma growth is dependent on glucose utilization and can be effectively inhibited by glucose antagonism.

Animals↗
PubMed1986

Plasminogen activator inhibitor from human fibrosarcoma cells binds urokinase-type plasminogen activator, but not its proenzyme.

An approximately 75% pure form of a human Mr approximately 54,000 plasminogen activator inhibitor from conditioned culture fluid of the fibrosarcoma cell line HT-1080 was obtained by a single step of chromatography on concanavalin A-Sepharose. The inhibitor inhibited human urokinase-type plasminogen activator (u-PA) and tissue-type plasminogen activator, but not plasmin. Rabbit antibodies against this plasminogen activator inhibitor also reacted with a plasminogen activator inhibitor with identical electrophoretic mobility in extracts of human blood platelets, indicating that the HT-1080-inhibitor is of the same type as the inhibitor of blood platelets. As revealed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis followed by fibrin-agarose zymography, incubation of HT-1080-inhibitor with the active form of human u-PA led to the formation of an equimolar sodium dodecyl sulfate-resistant complex between them; in contrast, no complex formation was observed between the inhibitor and the proenzyme form of human u-PA (pro-u-PA). Likewise, using a column of anti-inhibitor antibodies coupled to Sepharose for removal of excess inhibitor and activator-inhibitor complexes, the potential enzymatic activity of pro-u-PA was found to be unaffected by incubation with inhibitor under conditions in which more than 95% of the active u-PA had formed complex with inhibitor.

Cell Line↗
PubMed1986

Differences of host immune response and of sensitivity to chemotherapeutic agents between two clones of rat fibrosarcoma with different metastatic potential.

Differences of host immune response and of chemosensitivity between two clones derived from a methylcholanthrene-induced rat fibrosarcoma and exhibiting different tumorigenic and metastatic potentials were examined. Clone G, which has no metastatic potential, was more sensitive to natural killer cytotoxicity by syngeneic rat spleen cells than clone A, which is highly metastatic. The colony formation of clone G was strongly inhibited by the supernatant obtained from coculture of lymphocytes with either of these two clones. In contrast, the colony formation of clone A was not inhibited by these supernatants. Inhibition of the colony formation of clone G was dependent on the dilution of the supernatant and the incubation time of the lymphocytes and tumor cells used to generate the supernatant. The supernatant from cocultures of lymphocytes and clone G inhibited the colony formation of clone G more strongly than the supernatant from cocultures of lymphocytes and clone A. There was no difference between these two clones in chemosensitivity to seven of the ten chemotherapeutic drugs tested.

Animals↗
PubMed1986

Expression of H-2 antigens and inducibility of antitumor immune responses in various tumor cell clones established from methylcholanthrene-induced fibrosarcomas.

A large number of fibrosarcoma cell lines was established in vitro from a tumor mass induced freshly by inoculating 3-methylcholanthrene (MCA) subcutaneously (sc) into C3H/HeN mice, and more than five clones were isolated from each cell line by the limiting dilution technique. The present study investigated a) qualitative and quantitative comparison of the immunogenicity [tumor-associated transplantation antigen (TATA) activity] of different tumor clones and b) the relationship between such immunogenicity and the expression of H-2 class I antigens. When TATA were compared between different clones from the same tumor, these TATA were revealed to be cross-reactive to each other. On the other hand, the comparison of TATA between clones from different tumors demonstrated the existence of individually unique TATA in these clones. In addition to qualitative heterogeneity of TATA from different tumors, the magnitude of immunogenicity was also heterogeneous in the individual clones established. Whether or not such quantitative heterogeneity of immunogenic strength was related to the expression of H-2 (class I) antigens was examined by flow microfluorometry studies using anti-H-2k antibodies. The results demonstrated that there was no correlation between TATA activity capable of inducing in vivo tumor resistance and the expression of H-2 antigens. This contrasted with parallelism between the expression of H-2 antigens and inducibility of cytotoxic T lymphocytes (CTL) or lysability of tumor cell clones by CTL. These results are discussed in the context of the cellular mechanism of tumor cell eradication in vivo and the regulation of cell surface H-2 expression in vitro and in vivo.

Animals↗
PubMed1988

Differential extraction of tumor-specific antigens from two ultraviolet light-induced murine fibrosarcomas with the use of 1-butanol.

The purpose of this study was to investigate the immunobiological characteristics of the tumor-specific cell surface antigen expressed by the UV-induced murine fibrosarcoma, UV-2240. UV-2240 is classified as a regressor UV tumor because it is immunologically rejected by normal syngeneic mice but grows in immunocompromised or UV-irradiated hosts. The strong tumor-specific rejection antigen expressed by UV-2240 was found on the plasma membrane, and unlike the previously characterized antigen of UV-1591, the UV-2240 antigen was removed by using the noncytolytic butanol extraction technique. The tumor antigen activity in butanol extracts was resistant to digestion by endoglycosidase F and alpha-mannosidase, but was destroyed by pronase. In addition, the immunoprotective activity in extracts of UV-2240 was thermostable. These data demonstrate that the UV-2240-specific tumor antigen possesses physicochemical properties distinct from those of its well-characterized counterpart UV-1591.

1-Butanol↗
PubMed1988

Effect of Schistosoma mansoni and cyclophosphamide on a mouse fibrosarcoma.

Groups of B10A mice bearing a fibrosarcoma were treated with agents that induce eosinophilia such as cyclophosphamide (CY) or Schistosoma mansoni antigen (SMA) or both, and the growth of their tumors was evaluated. Tumor growth was most markedly attenuated in the group of mice that had 4 pairs of S. mansoni implanted in their backs 5 days before injection of tumor cells and then received SMA twice a week. These animals had tumor growth reduced by 90%. CY alone had no effect on tumor growth. In groups treated twice a week with SMA alone or associated with CY on day -2, tumor growth was reduced by 26% and 40%, respectively.

Animals↗
PubMed1988

Proliferation kinetics of a murine fibrosarcoma during fractionated irradiation.

Accelerated growth of tumor clonogens during the course of fractionated irradiation has been considered one of the major causes of radiation treatment failure. Alterations in clonogen growth rate could occur through three basic mechanisms: changes in cell-loss factor, changes in cell-cycle time, and recruitment of previously quiescent cells into the proliferative pool. This study was designed to assess changes in the cell-cycle time of clonogens of a murine fibrosarcoma during fractionated irradiation using an artificial pulmonary micrometastasis model. Lung colonies of various ages (4 h, 1 day, or 4 days) were exposed to single doses of irradiation ranging from 5-13 Gy; the fraction of surviving colonies was used to determine the preirradiation growth kinetics. The growth kinetics during fractionated irradiation was derived from colony-survival data of 4-day-old micrometastasis exposed to single doses or to 2, 5, 9, and 15 fractions separated by 4, 12, or 24-h intervals. The size of dose fractions used ranged from 1.7 to 14 Gy. The estimated clonogen doubling times before irradiation and during overall treatment periods of up to 14 days were 0.71 and 1.1 days, respectively. This significant (P less than 0.0001) increase in the doubling time was most likely a consequence of lengthening of the overall cell-cycle time of the clonogens by radiation-induced division delay. This observation suggests that accelerated growth, when it occurs in some tumors during fractionated treatment, is the result of a decreased cell-loss factor or recruitment of quiescent cells, but not a shortening of the cell-cycle time of the clonogens.

Animals↗