Sarcoma arising in a bronchiogenic cyst.
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Bronchi↗
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Results for “SARCOMA, FIBROSARCOMA”
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PATHOLOGICAL ASPECTS OF SOFT PART SARCOMAS.
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Child↗
Low-grade sarcomas with CD34-positive fibroblasts and low-grade myofibroblastic sarcomas.
A subset of low-grade fibrosarcomas is composed of CD34-positive spindle cells. These include dermatofibrosarcoma, its morphologic variants, and its associated fibrosarcoma, solitary fibrous tumor, hemangiopericytoma and their malignant counterparts, and some cases of myxoinflammatory fibroblastic sarcoma. Dermatofibrosarcoma and related lesions are characterized by a t(17;22)(q22;q13) rearrangement resulting in fusion of the genes COL1A (17q21-22) and PDGFB1 (22q13). Solitary fibrous tumor displays varying cellularity and fibrosis and a peripheral hemangiopericytomatous pattern; most tumors formerly called hemangiopericytoma are now subsumed into the category of solitary fibrous tumor, although a few strictly defined examples are recognized; however, these are probably not composed of pericytes. Myofibroblastic malignancies are best identified by electron microscopy, with which varying degrees of differentiation, including the presence of fibronexus junctions, can be identified. Low-grade sarcomas showing myofibroblastic differentiation include myofibrosarcomas and inflammatory myofibroblastic tumors. Myofibrosarcomas are spindle cell neoplasms that occur in children or adults in the head and neck, trunk, and extremities as infiltrative neoplasms and that display a fascicular or fasciitis-like pattern with focal nuclear atypia and variable expression of myoid antigens. These sarcomas are prone to recurrence and a small number metastasize. Inflammatory myofibroblastic tumor (synonymous with inflammatory fibrosarcoma) is a neoplasm arising predominantly in childhood, and frequently in intraabdominal locations. It has spindle cells in fascicular, fasciitis-like and sclerosing patterns, with heavy chronic inflammation including abundant plasma cells. Many IMT have clonal chromosomal abnormalities involving 2p22-24, and fusion of the ALK gene with tropomyosin 3 (TPM3-ALK) or tropomyosin 4 (TPM4-ALK) is found in a subset.
Antigens, CD34↗
Structural patterns and histological behaviour of experimental sarcomas. I. General considerations, histology and histochemistry.
Methylcholanthrene-induced rat sarcomas were used as a model for the examination of morphological and cytological differentiations in tumours of the connective tissue. Particular attention was paid to the question how far these sarcomas are comparable to human connective tissue tumours. The histological examination yields a broad spectrum of mesenchymal differentiations ranging from undifferentiated anaplastic sarcomas over less differentiated fibrosarcomas and malignant fibrous histocytomas to well-differentiated fibrosarcomas, myosarcomas and haemangiopericytomas. It is worth mentioning that different histological structures can be encountered with one and the same tumour.
Animals↗
Mixed glioblastoma and sarcoma with osteoid-chondral tissue.
A 56-year-old man had a right temporal lobe tumor with calcification, which was removed surgically and treated with irradiation. The histology of the tumor was mixed tumor of glioblastoma and fibrosarcoma, and in the sarcoma portion osteoid-chondral tissue was found. With stains for proteoglycan and enzyme digestion tests, hyaluronic acid and chondroitin sulfate were demonstrated in the cartilage matrix. The positive reactivity of the proteoglycans to high iron diamine staining in the first surgical specimens changed to negative in the second and autopsy specimens. It is likely that the osteoid-chondral tissue derived from metaplastic change in sarcoma cells and in the later stage pleomorphism appeared.
Astrocytoma↗
Evidence for extensive methylation of ribosomal RNA genes in a rat XC cell line.
XC cell line was established from a rat fibrosarcoma induced by avian sarcoma virus. Analysis of ribosomal RNA genes in the DNA of this cell line indicated that there was a 3- to 4-fold increase in the number of the rDNA repeating units. [methyl-14C]Methionine labeling experiments as well as Southern blot analysis of the restriction endonuclease fragments showed extensive methylation of the cytosine residues in the rDNA. Further analysis by HpaII, HhaI and MspI suggested that the entire rDNA repeat unit was uniformly methylated in the recognition sequence for these enzymes. Parallel experiments with two other rat cell lines (rat embryo fibroblasts and adenovirus-transformed rat embryo cells) indicated no evidence of methylation in the rDNA.
Animals↗
Familial cerebral sarcomas.
Four cases of cerebral fibrosarcomas occurring in two families are reported. To our knowledge, no similar cases have been reported. Evidence that a heritable factor is involved in the genesis of some brain tumors is suggested by these cases.
Aged↗
[Fibroblastic sarcoma of the tibia; early diagnosis; results after two years].
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Early Diagnosis↗
Malignant hemangiopericytoma and other sarcomas with hemangiopericytoma-like pattern.
This clinicopathologic study concerns 19 cases of malignant hemangiopericytoma among 755 cases of soft tissue sarcomas. The age of the patients ranged from 18 to 76 years, with a median of 43 years. Tumors occurred on the trunk in 8, lower extremities in 5, the head in 3, and the retroperitoneum in 3. According to follow-up information, nine of the 19 patients had died. Histologically the tumor was characterized by its homogeneous vascular pattern, its uniform cell population and a wide range of cellular anaplasia. After extensive sampling of the tumors, a comparative light microscopy revealed differences in diagnostic histology between malignant hemangiopericytoma and other soft tissue sarcomas with a hemangiopericytoma-like vascular pattern. The frequency of appearance of such pericytoma pattern in different soft tissue sarcomas was as follows: 4/4 cases (100%) in extraskeletal mesenchymal chondrosarcoma, 11/14 (79%) in infantile fibrosarcoma, 27/45 (60%) in synovial sarcoma, 62/201 (30%) in malignant fibrous histiocytoma, 9/37 (25%) in malignant schwannoma and 6/72 (8%) in liposarcoma.
Adolescent↗
Focal adhesion kinase regulates syndecan-2-mediated tumorigenic activity of HT1080 fibrosarcoma cells.
Expression of syndecan-2, a transmembrane heparan sulfate proteoglycan, is crucial for the tumorigenic activity in colon carcinoma cells. However, despite the high-level expression of syndecan-2 in mesenchymal cells, few studies have addressed the function of syndecan-2 in sarcoma cells. In HT1080 fibrosarcoma cells, we found that syndecan-2 regulated migration, invasion into Matrigel, and anchorage-independent growth but not cell-extracellular matrix adhesion or proliferation, suggesting that syndecan-2 plays different functional roles in fibrosarcoma and colon carcinoma cells. Consistent with the increased cell migration/invasion of syndecan-2-overexpressing HT1080 cells, syndecan-2 overexpression increased phosphorylation and interaction of focal adhesion kinase (FAK) and phosphatidylinositol 3-kinase (PI3K), membrane localization of T-lymphoma invasion and metastasis gene-1 (Tiam-1), and activation of Rac. Syndecan-2-mediated cell migration/invasion of HT1080 cells was diminished when (a) cells were cotransfected with nonphosphorylatable mutant FAK Y397F or with other FAK mutants lacking PI3K interactions, (b) cells were treated with a specific PI3K inhibitor, or (c) levels of Tiam-1 were knocked down with small interfering RNAs. Furthermore, expression of several FAK mutants inhibited syndecan-2-mediated enhancement of anchorage-independent growth in HT1080 cells. Taken together, these data suggest that syndecan-2 regulates the tumorigenic activities of HT1080 fibrosarcoma cells and that FAK is a key regulator of syndecan-2-mediated tumorigenic activities.
Cell Line, Tumor↗
[Radiotherapy of the soft tissue sarcomas (author's transl)].
Although 82,5% of the total body weight consist of mesenchymal tissues, only 1%--3% of all malignant tumors are soft tissue sarcomas. The necessary irradiation dose can only be determined after an exact histopathological diagnosis; therefore this diagnosis has to be made prior to the radiotherapy. Except the fibro- and liposarcomas, all sarcoma form very early lymphogenic metastases. All sarcomas show a remarquable tendency to form recurrences. Surgery is the primary therapy. After that, an irradiation of the tumor region and the regional lymph nodes should be effected under all circumstances. We have treated and checked up 749 patients. After this therapeutic method, the five-year survival rate in the stages T1 and T2 is 60% for the myxosarcoma, 67% for the angiosarcoma, 41% for the fasciculated sarcoma, 40% for the globocellular sarcoma, 30% for the polymorphous sarcoma, 69% for the fibrosarcoma, and 61% for the leiomyosarcoma.
Fibrosarcoma↗
Absence of SYT-SSX fusion products in soft tissue tumors other than synovial sarcoma.
The chromosomal translocation t(X;18), which generates SYT-SSX1 and SYT-SSX2 fusion products, is a sensitive marker for synovial sarcoma; most synovial sarcomas test positive for this marker. However, few studies have addressed the presence of t(X;18) or its fusion products in spindle cell sarcomas in the differential diagnosis of synovial sarcoma. We studied the presence of the SYT-SSX fusion products with reverse transcriptase polymerase chain reaction on frozen tissue samples of 24 synovial sarcomas and 24 other spindle cell sarcomas, including 12 malignant peripheral nerve sheath tumors. In cases histopathologically diagnosed as synovial sarcoma, SYT-SSX fusion products were detected in 21 of 24 (87%) lesions. No evidence of these fusions was found in 12 malignant peripheral nerve sheath tumors, 2 hemangiopericytomas, 3 leiomyosarcomas, 2 fibrosarcomas, 1 poorly differentiated sarcoma (malignant fibrous histiocytoma), 1 sarcoma with rhabdoid features, and 2 sarcomas not otherwise specified. One lesion with histologic, immunohistologic, and ultrastructural features indeterminate for a diagnosis of synovial sarcoma or malignant peripheral nerve sheath tumor was studied and was positive for SYT-SSX1. The SYT-SSX fusion products appear specific for synovial sarcoma and are not seen in other spindle cell lesions in its differential diagnosis.
Adult↗
The effect of tumour growth on liver pantothenate, CoA, and fatty acid synthetase activity in the mouse.
Enzymatic, and microbiological assays were used to determine the hepatic contents of coenzyme A, acetyl CoA, fatty acid synthetase activity, and pantothenate in livers of tumour-bearing mice. Significant decreases in CoA and acetyl CoA were found in mice bearing TLX-5 lymphoma, sarcoma 180 or a fibrosarcoma. These changes were accompanied by significant decreases in pantothenate and increases in 4-phosphopantothenate suggesting an increase in pantothenate kinase activity due to reduction of CoA inhibition of the enzyme. In contrast, large increases were found in pantothenate and 4-phosphopantothenate in mice bearing TLX-5 lymphoma, i.p. or s.c. These changes could be due to a large reduction in the rate of conversion of an intermediate in the pathway of CoA, or increased production of pantothenate or 4-phosphopantothenate from the degradation of CoA or the phosphopantetheine residue in fatty acid synthetase. Activities of fatty acid synthetase in liver of mice bearing this tumour showed marked decreases, but were insufficient to account for the increase in pantothenate, and may reflect a reduction in cytosolic CoA needed for the conversion of the apo to the holoenzyme.
Acetyl Coenzyme A↗
Bone cancers.
BACKGROUND: Frequency distribution data for primary bone sarcomas have long been used to provide clues to the diagnosis of bone cancers after their identification in radiographs. Age and skeletal site are often helpful, in addition to specific radiographic features, in narrowing down the probable histologic categories of bone neoplasms before biopsy. METHODS: Data on 2627 histologically confirmed primary malignant tumors of bone, as collected by the SEER program during the period 1973-1987, were analyzed by age, sex, race, and anatomical site. RESULTS: Osteosarcoma was the most frequently diagnosed primary sarcoma of bone (35.1%), followed by chondrosarcoma (25.8%), Ewing's sarcoma (16.0%), chordoma (8.4%), and malignant fibrous histiocytoma, including fibrosarcoma (5.6%). The most frequently diagnosed sarcoma of bone in persons younger than age 20 was osteosarcoma, followed by Ewing's sarcoma. Chondrosarcoma was the most frequently diagnosed bone tumor in the population older than age 50. The overall 5-year relative survival rates were as follows: osteosarcoma, 41.0%; chondrosarcoma, 72.7%; Ewing's sarcoma, 41.2%; chordoma, 63.8%; and malignant fibrous histiocytoma, 42.9%. There was an improvement in the survival rates during the period 1973-1987 for patients with chordoma and for white female patients with Ewing's sarcoma. Ewing's sarcoma and chordoma occurred almost exclusively in the white population. CONCLUSIONS: SEER data provide a unique opportunity to evaluate the incidence and survival rates of bone sarcomas, which are uncommon but highly lethal tumors. The findings from this analysis provide information useful in the diagnosis of these cancers.
Adolescent↗
The diagnosis and prognosis of synovial tumors in dogs: 35 cases.
Although synovial cell sarcoma is reported to be the most common neoplasm of the canine synovium, this retrospective study of 35 canine synovial tumors found that the majority were of histiocytic origin. Five (14.3%) synovial cell sarcomas were identified by positive immunohistochemical staining with antibodies to cytokeratin. Eighteen (51.4%) histiocytic sarcomas were identified by cell morphology and immunohistochemical staining with antibodies to CD18. Six (17.1%) synovial myxomas were identified by histologic pattern. The remaining six (17.1%) synovial tumors represented a variety of sarcomas, including two malignant fibrous histiocytomas (actin positive), one fibrosarcoma, one chondrosarcoma, and two undifferentiated sarcomas. Rottweilers were overrepresented in the histiocytic sarcoma category and Doberman Pinschers were overrepresented in the synovial myxoma category. The average survival time was 31.8 months for dogs with synovial cell sarcoma, 5.3 months for dogs with histiocytic sarcoma, 30.7 months for dogs with synovial myxoma, and 3.5 months for dogs with other sarcomas. Among the dogs with follow-up information available, metastatic disease was detected in 25% of dogs with synovial cell sarcoma, in 91% of dogs with histiocytic sarcoma, in none of the dogs with synovial myxoma, and in 100% of dogs with other sarcomas. Immunohistochemical staining for cytokeratin, CD18, and smooth muscle actin is recommended to make the diagnosis and thereby predict the behavior of synovial tumors in dogs.
Amputation, Surgical↗
Obligatory wounding requirement for tumorigenesis in v-jun transgenic mice.
Avian sarcoma virus 17 induces fibrosarcomas in chickens and can transform a number of avian cell types in vitro by the action of v-jun. This gene and the related cellular genes c-jun, jun B and jun D, encode transactivating (or repressing) DNA-binding proteins that form homo- or heterodimeric (Jun-Jun and Jun-Fos) complexes which recognize the AP-1 consensus sequence TGACTCA, a response element that confers sensitivity to the tumour-promoting phorbol ester TPA. We have produced several lines of transgenic mice carrying the v-jun oncogene, driven by the promoter of the widely expressed H-2KK major histocompatibility complex (MHC) class I antigen gene. Transgenic animals are initially phenotypically normal, but after full-thickness wounding they show abnormal wound repair, characterized by hyperplastic granulation tissue. Many of these lesions are slowly progressive because of continuing fibroblast proliferation, and over 2-5 months some give rise to dermal fibrosarcomas. This reproducible multistep transition through a proliferative but benign intermediate is associated with characteristic increments in v-jun expression. Moreover, hyperplastic wound repair and its progression are both related to transgene dosage, suggesting that there exists a quantitative requirement or threshold for v-jun action. Our results indicate that v-jun is not oncogenic in transgenic mice as a result of a 'single-hit' mechanism, but rather, in addition to an obligatory wound, that secondary genetic or epigenetic events (possibly conscripting normal constituents of wound repair) are necessary for tumour development and progression.
Animals↗
Host-mediated antitumor activity of Lactobacillus casei in mice.
Antitumor activity of Lactobacillus casei YIT 9018 ( LC9018 ) was studied in BALB/c mice by using two syngeneic tumors; methylcholanthrene-induced tumor (Meth A fibrosarcoma) and Kirstein murine sarcoma virus-transformed BALB/3T3 ( K234 tumor). Administration of an LC9018 -Meth A cell mixture induced complete suppression of the tumor growth, while simultaneous injections of LC9018 and Meth A cells into different sites had no suppressive effect on the tumor growth. Administration of the mixture subsequently induced specific transplantation immunity to the challenge tumor, which started to be generated on about the 5th day after the administration and continued to at least the 30th day. Administration of an LC9018 - K234 cell mixture also induced suppression of the tumor growth and generated specific antitumor immunity. Neutralization (Winn type) tests showed that T lymphocytes possessed tumor cytotoxicity but humoral immune serum did not, suggesting that the T cells with LC9018 -potentiated antitumor immunity functioned in the suppression of the tumor growth.
Animals↗
The role of chemotherapy in childhood soft tissue sarcomas other than rhabdomyosarcomas: experience of the Northern Israel Oncology Center.
Forty-three children with nonrhabdomyosarcomatous soft tissue sarcomas (NRSTS) were treated at the Northern Israel Oncology Center in Haifa, Israel, from 1971 to 1996. The male:female ratio was 1.5:1 and the median age of patient was 10 years (range, 3 months-18 years). The most common histopathologic diagnoses were fibrosarcoma (32.5%) and synovial sarcoma (16%). The sites of primary tumor were lower limb (35%), trunk (18%), upper limb (16%), head and neck (16%), and retroperitoneum (11%). By Intergroup Rhabdomyosarcoma Study classifications, 13 patients presented as group I, 15 patients as group II, 10 patients as group III, and 5 patients as group IV. Median follow-up time was 63 months (range, 6 months-18 years). The estimated survival after a 5-year period is 72% (SE +/- 17) for patients in group I, 75 +/- 15% in group II, 90 +/- 9% for patients in group III, and 40 +/- 21% for patients in group IV. Eleven patients relapsed; 4/6 who developed local relapse were cured and are alive with disease, while 4/5 who developed distant metastases are dead. For the 28 patients who underwent complete resection at diagnosis, the estimated survival after a 5-year period is 87 +/- 5% vs. 60 +/- 17% for the 15 patients who underwent partial excision or biopsy. Local radiotherapy was delivered after surgery to group III patients. Preoperative and postoperative chemotherapy was delivered to the patients of groups III and IV, and postoperative chemotherapy only to group II patients. Chemotherapy produced demonstrable gain in survival for group II and III patients but not for patients with metastases. The authors conclude that an aggressive surgical approach is needed in patients with NRSTS. Chemotherapy may help as a preoperative treatment in bulky disease or as a postoperative treatment for microscopic residual disease.
Adolescent↗