PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “SARCOMA, 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 1,351 records · Page 75Linked to original sources
PubMedDate not supplied

Trace element changes in serum and skeletal muscle compared to tumour tissue in sarcoma-bearing rats.

Cancer cachexia is characterized by wasting of the lean tissue and profound changes in the body composition of the tumour host. These changes are partly explained by an inefficient energy production but other factors may also be important, such as deficiency of essential nutritional components. In the present study the changes of trace elements in serum and skeletal muscle were compared to those in tumour tissue during tumour progression in sarcoma--bearing rats. Trace element analysis was performed directly on serum specimens and frozen sections from skeletal muscle and tumour tissue. The samples were analysed by energy dispersive X-ray fluorescence spectrometry (EDXRF) without any other pre-treatment such as homogenization and extraction. In skeletal muscle an increased content of zinc was found during tumour progression. The iron concentration was unchanged, but since muscle wasting is part of the cachexia this means that iron was transferred to other compartments. Thus the iron content of serum was doubled and tumour tissue had a high concentration of iron. Selenium was below detection limits in skeletal muscle but well detectable in tumour tissue and it increased during tumour growth. Rubidium and potassium content correlated in all tissues (R:0.98) as did bromine and sodium (R:0.98). Copper behaved differently from the other trace elements and showed large variability. This was also true when tissue copper was individually correlated to all other trace elements in the same tissue.

Animals↗
PubMed2005

Sarcomas: rare primary malignant tumors of the thorax.

In this article, it is aimed to review the radiological signs of unusual primary malignant tumors of the thorax. Radiological studies of 11 patients with histologic diagnosis of thoracic sarcomas were interpreted retrospectively. Tumors originated from the chest wall (n=3), mediastinum (n=4), and pulmonary parenchyma (n=4). Histopathologic diagnoses were fibrosarcoma (n=1), alveolar rhabdomyosarcoma (n=1), malignant hemangiopericytoma (n=1), malignant fibrous histiocytoma (n=2), pulmonary vein leiomyosarcoma (n=1), pulmonary artery sarcoma (n=2), pleuropulmonary blastoma (n=1), and chondrosarcoma (n=2). In order to evaluate thoracic sarcomas, cross-sectional methods such as CT and MRI can be useful in demonstrating the origin of the mass, relationship with and involvement of adjacent structures. They present as masses and, unfortunately, radiological findings are not sufficient for specific diagnosis.

Humans↗
PubMed1992

Isolation of the avian transforming retrovirus, AS42, carrying the v-maf oncogene and initial characterization of its gene product.

A novel avian transforming retrovirus was isolated from a chicken musculoaponeurotic fibrosarcoma. This virus (called AS42) induces tumors histopathologically indistinguishable from the original sarcoma after a long latent period when inoculated into newborn chickens. AS42 also exhibits a weak transforming activity when infected into chicken embryo fibroblasts (CEF). This virus is replication-defective and associated with a helper virus of subgroup A (called ASAV). An AS42-specific protein of about 100 kDa was immunoprecipitated from lysates of AS42-transformed CEF with antiserum directed against avian retrovirus virion proteins. Molecular analysis of the genomic structure of the AS42 virus has revealed that this 100-kDa protein represents a novel oncogene, v-maf of cellular origin, which is fused with a part of the viral gag gene (Nishizawa et al., Proc. Natl. Acad. Sci. USA 86, 7711-7715, 1989). Interestingly, some size variation was observed among the gag-maf fusion proteins found in individual clones of transformed CEF. Consistent with this observation, Southern blot analyses and nucleotide sequence determination of several independent isolates of proviral DNA indicated that this virus segregates multiple forms of deletion mutants, probably through homologous recombinations among the repetitive sequences present within the v-maf coding region.

Animals↗
PubMed1989

A newly isolated avian sarcoma virus, ASV-1, carries the crk oncogene.

Avian sarcoma virus 1 (ASV-1) was isolated from a spontaneous sarcoma of an adult chicken. It is a replication-defective virus that induces fibrosarcomas in young chickens and oncogenic transformation in cultured chick embryo fibroblasts. The ASV-1 genome has been cloned in the lambda gt WES.lambda B vector from closed circular viral DNA extracted from infected cells. The nucleotide sequence of the oncogene insert in the ASV-1 genome has been determined. It is virtually identical to the sequence of the oncogene crk recently discovered in the avian sarcoma virus CT10. ASV-1 and CT10 are two independent retrovirus isolates carrying the crk oncogene.

Amino Acid Sequence↗
PubMed1988

Comparison of three recombinant murine leukemia viruses carrying the v-src oncogene of avian sarcoma virus: differences in in vitro transformation and in vivo pathogenicity.

We previously described a recombinant Moloney murine leukemia virus (Mo-MuLV) carrying the v-src oncogene, Mo-MuLV(src). Mo-MuLV(src) encodes a gag-src fusion protein, transforms cells in culture, and induces fibrosarcomas in vivo. To compare transforming properties of the gag-src fusion protein to pp60src encoded by Rous sarcoma virus, we constructed a new recombinant virus, Mo-MuLV(+ src). Mo-MuLV(+ src) encodes pp60src in the context of Mo-MuLV. Cells transformed by Mo-MuLV(+ src) were round and formed colonies in soft agar, whereas Mo-MuLV(src)-infected cells were fusiform and did not grow in suspension. Thus, the extent of transformation induced by Mo-MuLV(+ src) was greater than that induced by Mo-MuLV(src). Subcutaneous inoculation of either virus into neonatal NIH Swiss mice resulted in fibrosarcomas at the site of injection. Further studies indicated that tumors induced by Mo-MuLV(+ src) grew rapidly but rarely metastasized. In contrast, tumors induced by Mo-MuLV(src) grew somewhat more slowly but metastasized with a high frequency (60%). These viruses may provide a useful model system for tumor metastasis. Another src-containing virus was also studied, MRSV (constructed by Anderson and Scolnick). MRSV also encodes pp60src but in the context of amphotropic MuLV. When injected intravenously into six-week-old mice, MRSV induced splenomegaly and spleen foci but no solid tumors, as reported previously. In contrast, Mo-MuLV(src)-induced fibrosarcomas mostly in the spleen under the same inoculation protocol. These results suggest that the v-src oncogene was the major pathogenic determinant in neonatal mice for all three src-containing viruses; however, variations in the nature of the transforming protein modulated the behavior of the induced tumors. In adult mice, greater differences in pathogenicity were observed.

Animals↗
PubMed1995

Nonrhabdomyosarcomatous soft tissue sarcomas of childhood: formulation of a simplified system for grading.

Because of the rarity of pediatric nonrhabdomyosarcomatous soft tissue sarcomas, it is difficult to test standardized treatment protocols for individual tumor entities. Grading has been used successfully to predict outcome of adult sarcomas, but pediatric soft tissue tumors display a notable difference in clinical behavior when compared to older patients. To test systematically a standardized treatment strategy for pediatric nonrhabdomyosarcomastous soft tissue sarcomas devised by the Pediatric Oncology Group, the authors devised a grading schema using concepts of adult grading systems and integrating the unique clinical and morphologic features of pediatric sarcomas. Three grading tiers were devised: Grade I, which includes certain pediatric tumors with little propensity for malignancy; Grade II, which is composed of tumors excluded from Grades I or III by virtue of histologic diagnosis and having <5 mitoses/10 high-power fields or <15% geographic necrosis; and Grade III, which comprises certain tumors known to be clinically aggressive by virtue of histologic diagnosis and non-Grade I tumors with >4 mitoses/10 high-power fields or > 15% necrosis. An initial retrospective analysis on a series of lesions treated at a single institution indicated a strong predictive value for grading. Subsequent prospective studies by the Pediatric Oncology Group continue to verify the prognostic value of pediatric nonrhabdomyosarcomatous soft tissue sarcoma grading, and studies on individual pediatric nonrhabdomyosarcomatous soft tissue sarcomas, such as synovial sarcoma, also indicate the relatively poor outcome of higher grade lesions. Grade can be used to predict outcome of pediatric nonrhabdomyosarcomatous soft tissue sarcomas and to devise treatment strategies for experimental protocols.

Adolescent↗
PubMed2004

Sarcomas of the oral and maxillofacial region: a review of 32 cases in 25 years.

Thirty-two cases of sarcomas involving the oral and maxillofacial region over a period of 25 years were reviewed. The age range was from 5 months to 77 years with a mean age of 42. The male to female ratio was 3:1. The sarcomas were located in the maxilla including the maxillary sinus (n= 13), mandible (n= 13), buccal mucosa (n= 3), temporomandibular fossa (n= 2), and submandibular region (n= 1). Histologically sarcomas were classified as osteosarcoma (n= 9), malignant fibrous histiocytoma (n= 7), rhabdomyosarcoma (n= 5), fibrosarcoma (n= 3), plasmacytoma (n= 2), leiomyosarcoma (n= 2), angiosarcoma (n= 2), liposarcoma (n= 1), and ameloblastic fibrosarcoma (n= 1). Surgical resection was performed in 29 cases. Local recurrence was found in 10 patients and metastasis in 11 patients. Metastases included five regional lymph node metastases and eight distant metastases. The survival of patients with local recurrence or metastasis was poor. Surgery is the most reliable treatment for sarcomas of the oral and maxillofacial region. Adequate excision with safety surgical margin as the initial therapy is important for better survival. The value of radiation therapy and/or chemotherapy is uncertain. The 5-year survival rate of primary cases was 61%.

Adult↗
PubMed1985

Aortic intimal sarcoma with embolic metastases.

A 46-year-old woman died from massive bowel infarction. At autopsy, a primary sarcoma was found growing along the intimal surface of the aorta at the level of the celiac axis. Tumor emboli were found in distal aortic branches and most abdominal organs. Immunoperoxidase for Factor VIII and electron microscopy (EM) did not support an endothelial origin. EM showed myofibroblastic differentiation. Review of the literature yields an array of diagnostic histologic terms for these tumors, hampering case comparison. The literature does suggest, however, that the clinical presentation of these rare neoplasms correlates nicely with the location and gross morphology of the lesion. We therefore propose a clinicopathologic classification, categorizing the lesions as intimal (obstructive and nonobstructive) and mural. The former are typically pleomorphic sarcomas and are probably of myofibroblastic origin, whereas the latter are usually leiomyosarcomas or fibrosarcomas that probably originate in the media or adventitia.

Aorta, Abdominal↗
PubMed1994

Malignancies in fibrous dysplasia.

BACKGROUND: Malignancies in fibrous dysplasia are rare. Most cases have been published as single case reports. The role of radiation therapy in the occurrence of sarcoma in fibrous dysplasia is still controversial. METHODS: The Mayo Clinic files were reviewed, including Mayo Clinic cases and consultation cases, to collect all cases of sarcomas arising in fibrous dysplasia. RESULTS: Among 1122 cases with a histologic diagnosis of fibrous dysplasia, 28 cases of sarcoma were found. These 28 cases included 16 Mayo Clinic cases and 12 consultation cases. The sarcomas occurred in 19 cases of monostotic fibrous dysplasia and 9 cases of polyostotic disease (only 1 of Albright's syndrome). The most common histotype was osteosarcoma (19 cases), followed by fibrosarcoma (5 cases), chondrosarcoma (3 cases), and malignant fibrohistiocytoma (1 case). Of the 28 patients, 13 (46%) had received radiation therapy before the sarcoma developed. Most of these sarcomas occurred in the craniofacial bones (13 cases) or in the proximal femur (7 cases), followed by the humerus, pelvis, tibia, and scapula. CONCLUSIONS: Prognosis was poor. Sarcomas may arise with or without radiation. Early diagnosis and adequate treatment may lead to improved prognosis.

Adolescent↗
PubMed1977

Abrogation of resistance to feline oncornavirus disease by immunization with killed feline leukemia virus.

Four-week-old specific-pathogen-free cats were immunized with a combined vaccine composed of killed feline leukemia virus and killed feline oncornavirus-associated cell membrane antigen-containing tumor cells. Immunization induced feline oncornavirus-associated cell membrane antigen antibody titers ranging from 1:32 to 1:256 but did not elicit detectable virus-neutralizing antibody titers. Kittens immunized with tumor cells alone developed higher feline oncornavirus-associated cell membrane antigen antibody titers (ranging from 1:512 to 1:2048) than those given the combined vaccine. All kittens were challenged with virulent Dynder-Theilen feline sarcoma virus at 12 weeks of age. Seventy-five % of the kittens vaccinated with combined vaccine and 67% of unvaccinated control kittens developed progressive fibrosarcomas after challenge. By contrast, none of the kittens vaccinated with killed tumor cells alone developed progressive fibrosarcomas after challenge. The combined vaccine did not, however, inhibit the induction of feline leukemia virus viremia.

Animals↗
PubMed1984

Antitumor activity of lentinan in murine syngeneic and autochthonous hosts and its suppressive effect on 3-methylcholanthrene-induced carcinogenesis.

The antitumor effect of lentinan in syngeneic and autochthonous tumor-host systems and its suppressive effect on 3-methylcholanthrene (MC)-induced carcinogenesis were confirmed using DBA/2 and SWM/Ms hosts. The regressive activity of lentinan against the solid form of Sarcoma 180 was the most effective in DBA/2, SWM/Ms, or A/J mice and less effective in C3H/He or C57BL/6 mice. The growth of a syngeneic MC-induced DBA/2.MC.CS-1 fibrosarcoma (native and trypsinized) was markedly inhibited, and the regression of tumors was detected by the i.p. injection of minute amounts of lentinan into DBA/2 mice, which were the most suitable host in lentinan treatment. When DBA/2 mice were used, lentinan was also effective for even autochthonous primary tumors induced within 15 weeks after MC inoculation, but less effective for tumors induced during the 16 to 36 weeks after MC treatment. Lentinan showed a prominent suppressive effect in MC-induced carcinogenesis using DBA/2 and SWM/Ms mice but not effect when BALB/c, C57BL/6, or C3H/He mice were used. The timing of lentinan administration in the latter result was examined using SWM/Ms mice, and lentinan, when it was given daily for 10 days after the third week of MC inoculation, was strikingly effective (33%), but not so effective (63%) when lentinan was given after the sixth week of MC treatment, compared with tumor-occurrence rate in the control group (88%). The reason why DBA/2, SWM/Ms, or A/J mice were suitable hosts for lentinan treatment is not clear, but the natural killer capability or phagocytic macrophage function in these strains seems to have no relation to lentinan action, because A/J mice are deficient in natural killer function, and in these strains of mice the phagocytic function of macrophages is weak. It may be quite possible that these strains of mice are most sensitive to delayed-type hypersensitivity and/or cytotoxic T-cell response in which T-cells and lentinan play important roles. The tumor-host systems presented here provide a good model in which lentinan retains an inhibitory capacity in syngeneic and autochthonous hosts, and such a model offers the possibility for further study of the host defense mechanism against cancer.

Animals↗