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At least 1,081 records · Page 60Linked to original sources
PubMed1984

Postirradiation malignant fibrous histiocytoma arising in juvenile nasopharyngeal angiofibroma and producing alpha-1-antitrypsin.

A fatal nasopharyngeal malignant fibrous histiocytoma developed in a young male after irradiation of juvenile nasopharyngeal angiofibroma diagnosed 5 years earlier. The sarcoma extended from the nasopharynx into the floor of the pituitary fossa and into both parasellar regions. There was no clinical evidence of any distant spread. Many of the malignant cells contained cytoplasmic granular and globular PAS-positive inclusions shown to be alpha-1-antitrypsin immunohistochemically. Ultrastructurally, this probably corresponded to electron-dense material with distinctive patterns and which had accumulated within distended ergastoplasmic cisternae of the neoplastic cells. Three previously reported case of postirradiation sarcomas arising in nasopharyngeal angiofibroma were said to be fibrosarcomas and none produced alpha-1-antitrypsin.

Adult↗
PubMed1992

[The ultrastructural and immunohistochemical observations of anaplastic meningioma].

Eighteen cases of anaplastic meningioma were studied by LM, EM and immunohistochemistry for vimentin, EMA, keratin, GFAP and S-100. Microscopically, there were four histologic types, i.e. fibrosarcoma-like, angiosarcoma-like, polymorphic giant cell sarcoma-like and angiopapillary structure. By EM, four kinds of cells: undifferentiated cell, intermediate transitional cell, spindle-shaped cell, and giant cell, were found and variant transitions from undifferentiated or poorly, differentiated to meningioma cells were observed. Their ultrastructures and immunohistochemical features are similar to those of malignant mesothelioma. Since these two kinds of neoplasm showed both mesenchymal and epithelial cells in the features, the authors consider that their histogenesis may also be similar.

Adolescent↗
PubMed1978

Investigations on the carcinogenic burden by air pollution in man. XVIII. The morphology of neoplasms induced in NMRI Mice after subcutaneous administration of PAH (individual or combination treatment).

A single s.c. dose of polycyclic aromatic hydrocarbons (PAH) administered individually or in combinations in the neck area to NMRI mice produced mainly malignant mesenchymal neoplasms at the injection site. Parts of these tumours frequently showed a high degree of polymorphism and, as a detailed examination of their morphology demonstrated were similar to sarcomas of the subcutaneous tissue observed in other animal models.

Air Pollutants↗
PubMed1980

[Radiogenic fibrosarcomas (author's transl)].

Two radiogenic fibrosarcomas are presented. One of them appeared 22 years after a radiotherapy because of carcinoma of the body of the uterus. Criteria for the distinction between radiogenic sarcomas and secondary tumors are given and discussed. The authors present a diagram of all radiogenic fibrosarcomas after mastocarcinoma quoted in the literature of the world. This renders possible a comparison between applicated doses and latent periods.

Adult↗
PubMed1991

[Correlation between epithelioid sarcoma and poorly differentiated fibroblastic synovialosarcoma].

The authors report an original case of tendosynovial sarcoma localizated in the side of the palm of the hand of an eight year old child. This tumor has two morphological forms. One is characteristic of undifferentiated synovialosarcoma, and the other of epitheloid sarcoma. The immuno-histochemical study confirms the diagnosis of undifferentiated synovialosarcoma. On the basis of this case and with reference to the literature, the authors suggest that epithelioid sarcoma and synovialosarcoma constitute the same entity.

Child↗
PubMed1989

Activation of pro-urokinase and plasminogen on human sarcoma cells: a proteolytic system with surface-bound reactants.

Human HT-1080 fibrosarcoma cells produce urokinase-type plasminogen activator (u-PA) and type 1 plasminogen activator inhibitor (PAI-1). We found that after incubation of monolayer cultures with purified native human plasminogen in serum-containing medium, bound plasmin activity could be eluted from the cells with tranexamic acid, an analogue of lysine. The bound plasmin was the result of plasminogen activation on the cell surface; plasmin activity was not taken up onto cells after deliberate addition of plasmin to the serum-containing medium. The cell surface plasmin formation was inhibited by an anticatalytic monoclonal antibody to u-PA, indicating that this enzyme was responsible for the activation. Preincubation of the cells with diisopropyl fluorophosphate-inhibited u-PA led to a decrease in surface-bound plasmin, indicating that a large part, if not all, of the cell surface plasminogen activation was catalyzed by surface-bound u-PA. In the absence of plasminogen, most of the cell surface u-PA was present in its single-chain proenzyme form, while addition of plasminogen led to formation of cell-bound two-chain u-PA. The latter reaction was catalyzed by cell-bound plasmin. Cell-bound u-PA was accessible to inhibition by endogenous PAI-1 and by added PAI-2, while the cell-bound plasmin was inaccessible to serum inhibitors, but accessible to added aprotinin and an anticatalytic monoclonal antibody. A model for cell surface plasminogen activation is proposed in which plasminogen binding to cells from serum medium is followed by plasminogen activation by trace amounts of bound active u-PA, to form bound plasmin, which in turn serves to produce more active u-PA from bound pro-u-PA. This exponential process is subject to regulation by endogenous PAI-1 and limited to the pericellular space.

Cell Line↗
PubMed1978

[The coincidence of Paget's disease and an immunoblastic sarcoma (author's transl)].

Malignant change is to be expected in about 1% of patients with Paget's disease. Usually these are osteosarcomas. Fibrosarcomas, benign and malignant giant cell tumours and chondrosarcomas are less common. The present case concerns the development of an immunoblastic sarcoma in the humerus, which was affected by Paget's disease. Only one other similar case is recorded in the literature. Other myelogenous tumours, such as plasmocytomas, are very rare in association with Paget's disease. Consequently there is no evidence for a causal connection between Paget's disease to these tumours, whereas sarcomas arising from bine tissue may be regarded as a form of malignant degeneration of Paget's disease.

Bone Marrow Diseases↗
PubMed1988

[Potentiation of chemotherapeutic activity by a Chinese herb medicine juzen-taiho-toh].

Antitumor activity of Juzen-Taiho-Toh (JTX) and combination effect of JTX with antitumor agents were studied using murine tumors. In order to determine the antitumor activity of JTX, mice inoculated ip with IMC carcinoma (1 X 10(6) cells/CDF1 mouse), sarcoma-180(1 X 10(6) cells/ICR mouse) or Meth-A fibrosarcoma (1 X 10(6) cells/BALB/c mouse) were treated with JTX (12.5-50 mg/kg/day) ip on day 1 through day 10, and the survival days of mice were examined. Treatment with 25 mg/kg/day produced 38.7% increase of life span against IMC carcinoma. However, no antitumor effect was observed on solid form of these tumors by the daily treatment with JTX. Combination effect of JTX and antitumor agents was also examined. ICR mice inoculated sc with 1 X 10(6) cells of sarcoma-180 on day 0 were treated with JTX (2,000 mg/kg/day) po on day-7 through day 30. In addition, some of these groups received mitomycin C (5 mg/kg), cytoxan (67 mg/kg) or adriamycin (2.5 mg/kg) iv on days 3, 8 and 11, and the size of tumor grown in sc site was measured by a caliper. In combination with JTX, mitomycin C resulted in a significantly greater tumor growth inhibition than could be obtained with mitomycin C alone. Secondly, BALB/c or C57BL/6 mice inoculated sc with 1 X 10(4) cells of Meth-A fibrosarcoma or 1 X 10(5) cells of B16 melanoma on day 0 were treated with JTX (2,000 mg/kg/day) po on day 1 through day 30. Some of these group received ip with mitomycin C (3 mg/kg), adriamycin (2 mg/kg), 5-FU (33 mg/kg) or cytoxan (67 mg/kg) on days 3, 6, 9, 12, 15 and 18. From this result, the group treated with JTX and mitomycin C also showed a higher tumor-growth inhibition. Thus, a combination of a high dose of mitomycin C with JTX was more effective than mitomycin C alone.

Animals↗