Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “FIBROSARCOMA”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

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

At least 235 records · Page 13Linked to original sources
PubMed1982

Protective effects of S-2-(3-aminopropylamino)ethylphosphorothioic acid against radiation damage of normal tissues and a fibrosarcoma in mice.

S-2-(3-Aminopropylamino)ethylphosphorothioic acid (WR-2721) was investigated for its protective effect against radiation-produced damage of jejunum, testis, lung, hair follicles, and a fibrosarcoma of C3Hf/Kam mice. Most of these tissues were radioprotected, and the degree of radioprotection depended on the dose of WR-2721 and the time interval between administration of WR-2721 and radiation treatment. WR-2721 increased resistance of jejunal epithelial cells and spermatogenic cells to single doses of gamma-rays by factors of 1.64 and 1.54, respectively. Protection against hair loss was less pronounced; the dose-modifying factor here was 1.24. The radiation-induced acute damage of the lung expressed by the increased formation of tumor nodules in the lung was not decreased by treatment of animals with WR-2721 before radiation. In contrast, WR-2721 augmented the radiation-induced enhancement of metastasis formation in the lung. WR-2721 protected fibrosarcoma micrometastases in the lung against therapeutic effect of radiation by a factor of 1.238. In contrast, this compound had no effect on the therapy of an 8-mm fibrosarcoma growing in the legs of mice.

Amifostine↗
PubMed1984

Antigenic variants isolated from a mutagen-treated guinea pig fibrosarcoma.

Antigenic variants were derived from a mutagen-treated, apparently nonimmunogenic fibrosarcoma of strain 2 guinea pigs. Fibrosarcoma line 107C3, originally induced by exposure of fetal cells to a chemical mutagen, was treated in vitro with the same mutagen. Cells that survived mutagen treatment were cloned, and the clones were tested for growth in soft agar, in conventional and immunosuppressed syngeneic guinea pigs, and in nude mice. At early passages after treatment, all clones tested in conventional syngeneic guinea pigs either failed to grow intradermally or grew temporarily and then regressed. At later passages after treatment, five of eight evaluable clones grew progressively; the characteristic of intradermal tumor growth followed by tumor regression (tum- or regressor) was a stable property of three of eight evaluable clones. The number of tumor cells required to produce progressively growing intradermal tumors in 50% of the animals (TD50) of the three tum- clones was at least 4 orders of magnitude greater than the TD50 of the parent fibrosarcoma. Tum- clones were not detected among 10 clones derived from the untreated parent tumor. Regressor clones formed colonies in soft agar and grew progressively in immunosuppressed syngeneic guinea pigs and nude mice. Regressor clones contained tumor transplantation antigens. Guinea pigs immunized with clones that grew and regressed rejected a challenge with the parent tumor when the dose of parent tumor cells was 1 to 3 times the TD50. Guinea pigs immunized by temporary growth of the parent tumor followed by excision of the local tumor and the regional lymph node did not reject a challenge with the parent tumor. These results confirm the results of experiments with murine tumors and extend the observations on tum- clones to the guinea pig. The results indicate that in guinea pigs it is possible by immunization with tumor cell variants derived from the mutagen-treated parent tumor to produce transplantation immunity to an apparently nonimmunogenic tumor.

Animals↗
PubMed1983

Primary pulmonary fibrosarcoma associated with Spirocerca lupi infection in a dog with hypertrophic pulmonary osteoarthropathy.

A dog with severe subperiosteal cortical thickening in all 4 limbs was found at necropsy to have a small noncircumscribed firm lesion in a lung lobe. Microscopically, the lung lesion was a fibrosarcoma that contained several adult nematodes identified as Spirocerca lupi. Lesions were not found in the esophagus or aorta, which are the typical locations for lesions caused by this parasite. Fibrosarcomas have been associated with S lupi infection in the esophagus. In this case, the nematode localized and reached maturity in an aberrant location and apparently participated in the development of a fibrosarcoma at this site.

Animals↗
PubMed1983

Monensin inhibition of hyaluronate synthesis in rat fibrosarcoma cells.

Evidence is presented that monensin-sensitive membranes, presumably the Golgi apparatus, are involved in the synthesis of hyaluronate in rat fibrosarcoma cells. Monensin caused the inhibition of incorporation of metabolic precursors into hyaluronate produced by rat fibrosarcoma cells in a concentration- and time-dependent manner. Maximum inhibition (70-80%) was obtained on treatment with 10(-7) M monensin for 24 h. Incorporation of label into secreted hyaluronate and into that associated with the cell surface was inhibited, but incorporation into intracellular hyaluronate was not inhibited. In 3T3 cells, treatment for 24 h with 10(-7) M monensin inhibited incorporation of label only into secreted hyaluronate. The hyaluronate-rich pericellular coat, revealed by exclusion of fixed red blood cells, was depleted on treatment with monensin under the same conditions which caused inhibition of hyaluronate synthesis in the fibrosarcoma cells. Cell proliferation, as measured by DNA content/culture and [3H]thymidine incorporation, was also inhibited in a dose-dependent manner by monensin (10(-8)-10(-6) M). Protein synthesis was not inhibited at these doses, nor was monensin cytotoxic as judged by a 51Cr release assay. The inhibition of hyaluronate synthesis was independent of the antiproliferative effect of monensin because it was obtained during log phase growth or confluency and in the presence or in the absence of serum.

Animals↗
PubMed1982

Soft tissue fibrosarcoma. A case report and review of the literature.

The soft tissue fibrosarcoma usually presents as an enlarging, painless mass. Pain is usually a result of pressure on surrounding structures. Fibrosarcomas arise from connective tissue and demonstrate no calcification on x-ray studies. These expansile tumors are firm, round or lobulated, and well encapsulated. Their level of malignancy is graded on the basis of various degrees of differentiation of the anaplastic spindle-cells of which they are composed. Treatment generally consists of wide excision or radical local resection. Five-year survival estimates vary from 60 to 90 percent. The lung is the usual site of metastasis. A case of subungual fibrosarcoma of the great toe is presented.

Aged↗
PubMed1981

Orthovoltage radiotherapy of oral fibrosarcomas in dogs.

Seventeen dogs with oral fibrosarcomas were referred for radiotherapy. All dogs were treated with orthovoltage x-rays at doses that approached the tolerance level of normal tissue. Acceptable normal tissue complications (epilation, mucositis, and moist desquamation) developed in all dogs surviving radiotherapy. Osteonecrosis, an unacceptable complication of radiotherapy, developed in 2 dogs. Of the 17 treated dogs, 2 died before radiotherapy was completed and 2 lived less than 1 month after treatment. One of the 17 was alive, with osteonecrosis, 27 months after radiotherapy and was free of tumor. The mean time to tumor regrowth and mean survival time in the other 12 dogs were 3.9 and 6.8 months, respectively. The results indicated a poor response of oral fibrosarcomas to treatment with orthovoltage x-rays. It was concluded that treatment of oral fibrosarcomas with other modalities, eg, 60Co gamma rays, may lead to improved results.

Animals↗
PubMed1981

Invasion of an artificial blood vessel wall by human fibrosarcoma cells.

Artificial blood vessel walls constructed by the addition of bovine arterial endothelial cells to multilayers of rat smooth muscle cells were used as substrates for the human fibrosarcoma cell line HT1080. The extracellular matrix proteins elaborated by the smooth muscle cells were prelabeled with [3H]-proline; therefore, their subsequent digestion could be followed by the appearance of radioactivity in the culture medium. The fibrosarcoma cells rapidly hydrolyzed smooth muscle multilayers in the absence of endothelial cells, but an endothelial layer markedly retarded the destructive ability of the tumor cells. The protective effect of the endothelium was not due to a lack of penetration of this cell layer, since HT1080 cells were observed by light and electron microscopy to be in the subendothelial area 24 hr after plating. Subsequently, the tumor cells multiplied in the region between the endothelial and smooth muscle layers and, although their degradative ability was retarded, they were ultimately capable of destroying the structure. Endothelial cells also inhibited hydrolysis of the smooth muscle layers if added simultaneously or up to 1 week after HT1080 cells, but the degree of inhibition was not as great as that seen with a preestablished endothelial layer. Measurable inhibition of tumor cell degradative activity was observed at fibrosarcoma:endothelial cell ratios of 25:1, demonstrating the potency of endothelial cells in modulating this aspect of the invasive phenotype. Although the HT1080 cells only slowly degraded the preexisting matrix proteins in artificial vessel wall cultures, they interfered with the production of new connective tissue proteins which occurred in control cultures. These experiments therefore suggest that endothelial cells have profound effects on tumor cell proteolytic activity, and the significance of these observations to tumor cell extravasation in vivo is discussed.

Animals↗
PubMed1981

Comparison of the chemotactic responsiveness of two fibrosarcoma subpopulations of differing malignancy.

There are several points of similarity between the processes of cancer metastasis and inflammation. In both, cells circulate in the vasculature, arrest, and cross vessel walls, thereby entering the extravascular tissues. In vitro, leukocytes and some, but not all, tumor cells exhibit chemotaxis. Since the chemotactic response of leukocytes effect their transvascular migration, we propose that chemotactic responsiveness contributes to the ability of circulating tumor cells to localize in extravascular tissues. This study was done to seek a relationship between chemotactic responsiveness of tumor cells and their behavior in vivo. Two subpopulations of cells were isolated from a methylcholanthrene-induced fibrosarcoma. The two cell lines were compared with regard to their biologic behavior in vivo and their chemotactic responsiveness in vitro. In vivo one subpopulation was highly malignant. An injection of 2.0 x 10(5) cells into the footpad of syngeneic mice led to the development of primary tumors in 87% of the animals and lung metastases in 61% of the animals with primary tumors. This line demonstrated chemotaxis to a factor that behaved similarly in gel filtration and showed immunologic reactivity similar to that of a previously described tumor cell chemotactic factor derived from the fifth component of complement. In contrast, an injection of the same number of cells from the second subpopulation of fibrosarcoma cells led to the development of primary tumors in only 12% of syngeneic mice, and lung metastases did not occur. Neither this subpopulation nor normal embryonic fibroblasts demonstrated chemotactic responsiveness. We postulate that the ability of tumor cells to respond to specific chemotactic stimuli may be one of the many unique properties which distinguish malignant from benign tumor cells. This is the first report documenting the chemotactic responsiveness of non-ascites tumors and fibrosarcomas.

Animals↗
PubMed1995

[A case of mediastinal fibrosarcoma].

Mediastinal fibrosarcoma is rare and comprises only 0.18% of mediastinal tumors. A case of mediastinal fibrosarcoma is reported. A 57-year-old woman was admitted to our hospital with a chief complaint of chest oppression. Computed tomogram and magnetic resonance imaging revealed an anterior mediastinal tumor expanding beneath the diaphragm. The tumor invaded the pericardium, the left lung and the diaphragm, so extensively resected. The resection was non-curative because of the presence of bloody pericardial effusion and maligant stump of the pericardium. Pathological examination showed fibrosarcoma. Although she recovered well postoperatively, she died with recurrence of the tumor, especially direct oppression of the heart, 8 months after the operation. In this case adjuvant chemotherapy did not effective and noncurative operation did not improve the prorhylaxis.

Female↗
PubMed1976

Effect of oil-attached BCG cell-wall skeleton on the induction of pleural fibrosarcomas in mice.

The effect of oil-attached BCG cell-wall skeleton on the induction of pleural fibrosarcomas by 3-methylcholanthrene in mice was examined. The pleural fibrosarcomas were induced by a substernal injection of 3-methylcholanthrene into the thoracic cavity of ddO mice. One week after the injection of 3-methylcholanthrene, 100 mug of oil-attached BCG cell-wall skeleton was injected subcutaneously every week for 10 weeks. In the observation period of 130 days, the incidence of pleural fibrosarcoma was 67% in the control mice and 39% in the mice treated with BCG cell-wall skeleton. The latent period of tumor induction was prolonged in the mice treated with BCG cell-wall skeleton.

Animals↗
PubMed1994

Complete regression of human fibrosarcoma xenografts after local Newcastle disease virus therapy.

We have recently demonstrated that a single local injection of the avian pathogen Newcastle disease virus (NDV; strain 73-T) causes complete regression of human neuroblastoma xenografts in athymic mice (R. M. Lorence, K. W. Reichard, B. B. Katubig, H. M. Reyes, A. Phuangsab, B. R. Mitchell, C. J. Cascino, R. J. Walter, and M. E. Peeples. J. Natl. Cancer Inst., 86: 1228-1233, 1994). In this report, we tried to determine if this in vivo antineoplastic effect of NDV extends to human sarcomas. Athymic mice with s.c. HT1080 fibrosarcoma xenografts (7-14 mm) were randomly divided into two groups and treated i.t. with a single injection of either 10(7) plaque-forming units of NDV or phosphate-buffered saline. Complete tumor regression occurred in 8 of 10 mice treated with NDV while unabated tumor growth occurred in all 9 mice treated with phosphate-buffered saline (P < 0.001). To determine if complete tumor regression was long lasting, the 8 mice were monitored for 1 year, during which time no tumor recurred. To test the antitumor effects of NDV on tumors derived from a fresh human sarcoma, a similar experiment was performed in athymic mice using TH15145 synovial sarcoma xenografts at their first and second passages. Of 9 mice with TH15145 xenografts, a single i.t. injection of NDV (10(7) plaque-forming units) caused complete regression of 3 tumors and > 80% regression in 3 more tumors. In contrast, tumors in all 5 mice treated with phosphate-buffered saline exhibited unabated growth (P < 0.03 for > 80% tumor regression). Since HT1080 fibrosarcoma cells express the N-ras oncogene, we explored the effects that transfection of this oncogene has on the sensitivity to NDV. Cultured human fibroblasts that were made tumorigenic following N-ras-transfection were found to be 1000-fold more sensitive to NDV than normal fibroblasts in a cytotoxicity assay. Oncogene expression by the HT1080 fibrosarcoma may therefore contribute to the long-lasting complete regression of this sarcoma following a single local injection of NDV.

Animals↗
PubMed1996

Retention of unmethylated CpG island alleles in human diploid fibroblast x fibrosarcoma hybrids expressing high levels of DNA methyltransferase.

The mechanisms underlying ectopic methylation of CpG islands in neoplastic cells are poorly understood. One determinant may be the increased expression of DNA methyltransferase (DNA MTase) observed frequently in neoplastic cells. To evaluate the role of DNA MTase overexpression in aberrant CpG island methylation, we assessed methylation of fibroblast-derived CpG islands in human diploid fibroblast x fibrosarcoma hybrid cell lines. Each of six independently derived, immortalized hybrid cell lines exhibited a high level of DNA MTase expression, comparable to that of the fibrosarcoma parental line. The methylation status of five CpG island loci, each of which was methylated extensively in the fibrosarcoma parental cells but not in the fibroblasts, was then determined in the hybrid cell lines. The patterns of methylation were consistent and highly locus dependent among the hybrid lines. Unmethylated alleles were retained stably at three loci. The parental origin of alleles could be determined at two other loci in the hybrid cells. Whereas no methylation of parental fibroblast-derived alleles of the HIC-1 locus was noted in hybrid cell lines, a marked increase in methylation of fibroblast-derived alleles of the estrogen receptor was observed in all hybrid cell lines. Therefore, despite high-level DNA MTase expression, widespread loss of unmethylated CpG islands was not observed in the hybrid cell lines. The nonrandom pattern of increased CpG island methylation in the hybrid cell lines suggests that locus-specific features and/or clonal selection, and not just DNA MTase expression, affect the evolution of ectopic methylation in neoplastic cells. Somatic cell hybrids may provide useful models for studying aberrant epigenetic events in neoplastic cells.

Alleles↗
PubMed1998

Inflammatory myofibroblastic tumor, inflammatory fibrosarcoma, and related lesions: an historical review with differential diagnostic considerations.

The concept of the inflammatory myofibroblastic tumor (IMT) has evolved from an already perplexing pathological process, the inflammatory pseudotumor, which was initially recognized in the lung and regarded as a pseudoneoplasm, although its histological features resembled a spindle cell sarcoma. Despite the pathological findings and their apparent prognostic implications, most affected individuals regardless of the primary site have had favorable clinical outcomes. The designation of inflammatory pseudotumor came to be widely accepted, although these lesions were clearly tumors or masses that may or may not have been pseudoneoplasms. An aberrant or exaggerated response to tissue injury without an established cause has generally been favored as the pathogenesis of the inflammatory pseudotumor or IMT. Once the myofibroblast was identified and its function in tissue repair was established, this cell type was found in a variety of soft tissue lesions from nodular fasciitis to malignant fibrous histiocytoma. The myofibroblast was eventually recognized as the principal cell type in the inflammatory pseudotumor, which provided the opportunity to redesignate this tumor as IMT. Some of the clinical and pathological aspects of the IMT began to suggest the possibility that these lesions are more similar to neoplasms than a postinflammatory process. Another step in the evolution of the inflammatory pseudotumor and IMT occurred with the report of a mesenteric or retroperitoneal tumor with similar pathological features to the latter tumors but with more aggressive behavior to warrant an interpretation of malignancy as an inflammatory fibrosarcoma. The IMT and inflammatory fibrosarcoma appear to have many overlapping clinical and pathological features. These tumors are histogenetically related, and if they are separate entities, they are differentiated more by degrees than absolutes. The therapeutic approach to these tumors should relay primarily on surgical resection. Studies in the future may possibly resolve the question whether the IMT and inflammatory fibrosarcoma are synonomous or closely related entities.

Diagnosis, Differential↗
PubMedDate not supplied

[Primary fibrosarcoma of the right ventricle].

Mexican literature has information of two fibrosarcomas in the atria. In the present work the first fibrosarcoma of the present work the first fibrosarcoma of the right ventricle found in Mexico is presented. This case behaved clinically, electrocardiographically, and phonomechanocardiographically like an Ebstein's disease, with the exception that in the phono a giant "a" wave was found. A review is mad of the clinical history, EKG, radiologic, and phono findings, as well as the laboratory analysis and data found in the autopsy.

Autopsy↗
PubMed1998

The salubrious effects of ascorbic acid on cyclophosphamide instigated lipid abnormalities in fibrosarcoma bearing rats.

The combined effect of cyclophosphamide and ascorbic acid on plasma lipids and lipoprotein profiles are important since, ascorbic acid encumbered the lipid abnormalities initiated by cyclophosphamide during cancer chemotherapy. Hence, the study was launched to appraise the salutary role of ascorbic acid in cyclophosphamide administered fibrosarcoma bearing rats. Fibrosarcoma cell line induced rats were treated with cyclophosphamide (10 mg/kg body weight) and ascorbic acid (200 mg/kg body weight) individually and in combination for 28 days. The concentration of plasma lipids and lipoprotein profiles were determined in control and experimental animals. The untreated, as well as cyclophosphamide administered fibrosarcoma bearing rats, divulged significantly increased levels of plasma total cholesterol, triglycerides, phospholipids, VLDL- and LDL-cholesterol, as compared with their respective control animals. In contrast, ester and HDL-cholesterol levels exhibited a marked decrease in these animals. Similar observations were also noticed in liver lipid values, as well. However, these lipid abnormalities were corrected by the co-administration of ascorbic acid. These results suggested, that some clinical entanglement of cyclophosphamide was refrained by co-administration of ascorbic acid in tumor stress condition.

Animals↗
PubMed1983

H-2K restriction of the T cell-mediated lysis of a chemically-induced BALB/c fibrosarcoma.

Previous work has shown that a cytotoxic T lymphocyte (CTL) immune response of syngeneic mice immunized with a chemically-induced BALB/c (H-2d) fibrosarcoma was directed against an individual tumour-associated antigen. To see whether this reaction was restricted by products of the major histocompatibility complex (MHC), anti-H-2 alloantisera to K or D antigens were used to interfere with the CTL-mediated immune response. Antisera to Kd but not to Dd antigens inhibited the lytic activity of CTL against fibrosarcoma cells. In addition, the study of the CTL response in F1 leads to P antitumour immunized chimeric mice showed that antitumour cytotoxicity developed only when F1 and parental host shared the Kd region. Both experiments strongly indicate that recognition of the individual tumour-associated antigen of the BALB/c fibrosarcoma is restricted by the products of H-2Kd genes.

Animals↗
PubMed1992

Fibrosarcoma of the breast: mammographic findings in five cases.

The mammographic features of fibrosarcoma of the breast, a rare malignant tumor, have not been described. Accordingly, we reviewed the mammograms, pathology reports, and medical records of five women with this tumor. All cases had surgical biopsies and a diagnosis made by histologic evaluation. The age of the patients ranged from 48 to 79 years. Histologically, three of the five fibrosarcomas were thought to have arisen from phyllodes tumor, and four were palpable. On mammograms, the tumors were dense masses with largely indistinct margins, ranging from 1.5 to 7.0 cm in diameter. One contained calcified osseous elements suggesting osseous trabeculae. Although the osseous trabeculae in that tumor strongly suggested sarcoma, most of the tumors had a nonspecific appearance on mammograms. Fibrosarcomas of the breast have a nonspecific mammographic appearance. Surgical biopsy and histologic evaluation are necessary for definitive diagnosis.

Breast Neoplasms↗
PubMedDate not supplied

Ameloblastic fibrosarcoma: report of a case. Immunohistochemical study and review of the literature.

Ameloblastic fibrosarcoma is a rare malignant odontogenic tumour characterized by a benign epithelial component within a malignant fibrous stroma. Its behaviour is relatively benign, with absence of metastatic disease, and the prognosis is reported to be good. It is a paradoxical neoplasm with "sarcomatous" morphological and immunohistochemical patterns but with a favourable clinical course. We report a new case of this tumour in a mandibular ramus of a 31-years-old male patient, that was surgically excised and treated with adjuvant chemotherapy and radiotherapy. Five years later the patient is free of disease. The growth potential of ameloblastic fibrosarcoma is evaluated and compared with a related lesion, the ameloblastic fibroma. The sarcomatous mesenchymal component of ameloblastic fibrosarcoma is positive to Ki67, PCNA and p53, in front of the negativity of ameloblastic fibroma.

Adult↗