Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1261473 (sarcoma)
 25,952 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Interrelationships between neoplastic progression and the expression of intermediate filaments were examined in primary cultures, immortal lines, and Kirsten murine sarcoma virus (KiMSV) transformed lines of rat ovarian surface epithelial (ROSE) cells. Immunofluorescence microscopy revealed abundant keratin filaments in all cells of primary cultures. In immortal, nontumorigenic lines, keratin filaments were detected in fewer cells, in smaller numbers, and in microscopically altered forms. The percentage of keratin-positive cells ranged from 4 to 54%. Its expression was inversely proportional to cell density. Keratin expression was similar in the two immortal lines, although one had retained a monolayered epithelial growth pattern resembling primary cultures, while in the other the growth pattern of the cells was more atypical. The two KiMSV-transformed lines were previously shown to produce tumors in vivo that resemble human ovarian endometrioid stromal sarcomas. In spite of this histologic appearance, the proportion of keratin-positive cells in these cells was increased over the immortal lines. Keratin expression was unrelated to cell density, and keratin in most virally transformed cells was limited to few, fine filaments. In thymidine-labelled immortal and virus-transformed cultures stained for keratin, no correlation was found between keratin expression and proliferative activity. The keratin profiles of primary and immortal cultures were identical on Western blots, with subtypes ranging from 52 to 66 kDa. The two virally transformed lines lacked some of the subtypes. Vimentin networks were faint or absent in primary cultures. In the immortal and the virus-transformed lines, neoplastic progression was associated with increasing vimentin expression but with no changes in filament morphology and distribution. The results show that the abnormalities in intermediate filament expression that accompany immortalization do not preclude the retention of a normal epithelial morphology and growth pattern in this cell type. Furthermore, the number of intermediate filaments and their intracellular distribution appear to be altered at an earlier stage in neoplastic progression than those mechanisms that select for specific keratin subtypes, or those that respond to regulation by cell density. Finally, the presence of keratin in the KiMSV-transformed lines examined in this study supports the hypothesis that human ovarian stromal sarcomas can arise in the OSE.
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PMID:Intermediate filaments in rat ovarian surface epithelial cells: changes with neoplastic progression in culture. 137 15

Seven cases of mixed glioblastoma multiforme (GBM) and sarcoma, or gliosarcoma (GS) and six cases of GBM with a prominent pilocytic or spindle cell component were studied with a panel of ten antibodies using the ABC method. All 13 cases were originally diagnosed as GS based on hematoxylin and eosin- (H&E) and reticulin-stained sections. In all GS, the glial component stained strongly for glial fibrillary acidic protein (GFAP), and most stained for S-100 protein, while the sarcomatous areas of GS did not stain for either of these antigens. This resulted in a characteristic, bimorphic marmorate staining pattern. In contrast, spindled GBM stained diffusely for GFAP and S-100 protein. Vimentin was detected in neoplastic glia of both GBM and GS and in the sarcomatous foci of GS. A spectrum of cytokeratins, Factor VIII, desmin and neurofilament were not detected in either GS or GBM. Actin, Leu 7 and alpha-1-antichymotrypsin were focally and inconsistently found in both GS and GBM. Perithelial spindle cell proliferations and intramural spindle cells within thick-walled vessels stained for GFAP, S-100 protein and/or vimentin. These studies confirm that GS is a true biphasic neoplasm that frequently cannot be distinguished from pilocytic or spindled GBM on routine histologic examination. Invasion of the dura, leptomeninges, and hyperplastic or hypertrophied blood vessels by malignant glial cells particularly confounds interpretation of H&E and reticulin stains. Immunohistochemical staining for GFAP complements the reticulin stain in confirming the presence of two cell populations in GS.
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PMID:Gliosarcoma: a histologic and immunohistochemical reaffirmation. 215 18

The immunohistochemical study of 60 cases of rhabdomyosarcomas made it possible to test eight different antibodies currently used in tumour pathology: i.e., antisera to vimentin, desmin, myoglobin, cytokeratin, epithelial membrane antigen, S100 protein, neurofilaments, and leukocyte common antigen. Vimentin was found in 58 cases (97 per cent), desmin in 49 cases (82 per cent), myoglobin in 23 cases (38 per cent), S100 protein in 7 cases (12 per cent), and cytokeratin in 3 cases (5 per cent). Other markers were negative. S100 protein was present in large round tumour cells with abundant eosinophilic cytoplasm (round rhabdomyoblasts), whereas cytokeratin was present in small tumour cells similar to those observed in rhabdoid sarcoma. This unexpected staining should become common knowledge for the correct interpretation of the immunohistochemical study of small cell tumours in the young.
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PMID:Immunohistochemical study of rhabdomyosarcoma. Unexpected staining with S100 protein and cytokeratin. 245 82

Ten examples of giant cell carcinoma of the lung were examined by immunohistochemistry for expression of keratin and vimentin intermediate filaments and for epithelial membrane antigen (EMA). Six cases were also examined electron microscopically. Keratin expression and, to a lesser extent, EMA immunoreactivity were reduced in comparison with better differentiated forms of lung carcinoma. Vimentin expression was increased, often taking the form of strong paranuclear staining. This may correspond to dense paranuclear aggregates of intermediate filaments seen ultrastructurally. Desmosomes were absent or sparse in most tumours. We propose that giant cell carcinoma arises by a process of dedifferentiation. The resulting loss of epithelial features gives rise to neoplastic cells which have features in common with some forms of sarcoma.
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PMID:Giant cell carcinoma of the lung--immunohistochemical and ultrastructural evidence of dedifferentiation. 245 72

We review 111 cases of rhabdoid tumor of kidney (RTK), including 79 entered on the National Wilms' Tumor Study (NWTS). Median age at diagnosis was 11 months, with a range from 0 to 106 months. The male:female ratio was 1.5:1. Gross features included a characteristic involvement of perihilar renal parenchyma. A wide histological spectrum was encountered, including nine major morphological patterns (classical, epithelioid, sclerosing, lymphomatoid, histiocytoid, etc.). These appearances invite confusion with other renal neoplasms. Ultrastructural studies were performed in 20 cases; immunocytochemical studies were performed in 11. Vimentin was demonstrated in all tumors; epithelial membrane antigen was seen in 7. Nonspecific decoration of cytoplasmic inclusions by a variety of immunostains was found in several cases. Several findings suggested that RTK might arise from primitive cells involved in formation of the renal medulla. There was no evidence of a histogenetic relationship to Wilms' tumor, although RTK may overlap with mesoblastic nephroma and clear cell sarcoma. Of the 70 NWTS patients with adequate follow-up, 56 (80%) have died. Every patient presenting with distant metastases died, whereas 10 of 20 with negative nodes survived. Survival rates were higher for girls (56.3% versus 11.1%). None of the histological variables had independent prognostic significance.
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PMID:Rhabdoid tumor of kidney. A report of 111 cases from the National Wilms' Tumor Study Pathology Center. 254 25

Primary tumor of the aorta is extremely rare. An instance of aortic intimal sarcoma, namely fibromyxosarcoma, which extended from the beginning of the descending aorta to 7 cm above the abdominal bifurcation, with clinical evidence of acutely occurring hypertension, arterial embolism of the lower extremities, renal infarction, and aortic occlusion in a 50-year-old male is reported. The tumor was limited to the intima and composed of spindle-shaped tumor cells with abundant myxoid extracellular matrices. The tumor cells were negative for Factor VIII, Desmin, or Myoglobin, but were positive for Vimentin or Factor XIIIa in immunoperoxidase studies. An electron microscopic examination revealed a large amount of rough endoplasmic reticulum in the cytoplasm. Parenchymal metastases were observed in both the lungs and thoracic vertebrae. A review of literature on the clinical and pathological aspects of the tumor was made.
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PMID:A case of aortic intimal sarcoma manifested with acutely occurring hypertension and aortic occlusion. 258 79

Gliosarcomas contain both neuro-ectodermal and mesenchymal elements. Its histogenesis has been much debated and endothelial and adventitial fibroblast origins have been suggested, as has a "histiocytic" origin following the demonstration of antiprotease activity. Eight gliosarcomas have been examined with a panel of ten monoclonal and polyclonal antibodies to investigate the origin of the sarcomatous element. Glial fibrillary acid protein expression showed a sharp distinction between gliomatous and sarcomatous tumour components. Contrary to some previous reports factor 8-related antigen and Ulex europeus agglutinin stained vascular luminal endothelium but no tumour cells. Vimentin and fibronectin expression was extensive and confined largely to sarcomatous areas. Desmin and neurofilament protein could not be demonstrated in any of the cases. Numerous cells, particularly in the sarcoma areas, expressed alpha-1-antitrypsin and -chymotrypsin. A proportion of these stained for the monocyte/macrophage marker MAC 387. Four cases focally exhibited a true storiform pattern and this and the immunohistochemical results suggest analogies with the fibrous histiocytomas. These tumours contain reactive histiocytes but are now thought to be derived from fibroblasts or from pluripotent mesenchymal cells in perivascular adventitia. This resembles the pattern exhibited in the sarcomatous component of gliosarcomas.
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PMID:Gliosarcoma: an immunohistochemical study. 260 37

Primary gastrointestinal T-cell malignant lymphomas (T-ML) are very rare. In this case report we describe a primary gastric tumor with local lymph node involvement. On the basis of histologic, immunohistochemical, and electron microscopic studies, the authors classified this tumor as a pleomorphic T-ML, large cell variant with peripheral helper/inducer T-cell phenotype (Leu1/CD5+, Leu4/CD3+, Leu5/CD2+, Leu9/CD7+, and Leu3/CD4+). The extreme pleomorphism of lymphoma cells, the numerous giant cells, and the presence of tumor nodules with two or three concentric layers were the three striking morphologic features of our case. Tumor cells showed an inconstant but true positive staining with anti-LeuM1/CD15 and LeuM3/CD14 antibodies. Vimentin positivity could be related to the presence of intermediate filaments at ultrastructural level. Neuron-specific enolase reactivity was a peculiar but unexplained feature. Furthermore, the positivity of the surface markers Ki-1/CD30, anti-Tac/CD25 and HLA-DR, and the nuclear marker Ki-67 suggested an activation state and a high proliferative activity of the tumor cells. This study emphasizes the usefulness of combined pathologic methods in order to rule other diagnoses such as undifferentiated carcinoma, malignant melanoma, malignant histiocytosis, B-cell lymphoma and interdigitating reticulum cells sarcoma, in view of an extremely polymorph tumor proliferation. This is apparently the first completely documented case report of a primary gastric pleomorphic T-ML of peripheral T-cell origin.
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PMID:Primary gastric peripheral T-cell malignant lymphoma with helper/inducer phenotype. First case report with a complete histological ultrastructural and immunochemical study. 296 94

Chordomas are slowly growing malignant tumors arising from notochordal rests. They are occurring in adults (50 to 60 year old) and are mainly (85%) located in sacrococcygeal or spheno-occipital regions; other main localization is cervical spine. Chordomas are usually discovered in patients with pain or symptoms due to compression of surrounding viscera. Radiologically it is characterized by association of osteolysis and soft tissues opacity. On macroscopic examination tumoral tissue has mucoid appearance; under microscope it is made up with lobules of epithelial-appearing cells surrounded by acid mucosubstances. Tumorous cells contain glycogen and neutral mucosubstances. They are surrounded by argyrophilic rim due to pericellular condensation of intercellular matrix, well viewed on electron microscope examination. When their cytoplasm is filled with vacuoles, cells take up typical physaliphorous appearance. Chordomas cells express epithelial differentiation antigens (low molecular weight cytokeratins, EMA, CAM 52, HFM 62, even CEA), Vimentin and S-100 Protein: this triple positivity allow differentiation between chordomas and numerous others tumors. Correct treatment of chordoma is achieved with an initially complete excision. Local recurrences are frequent and sometimes inoperable: in this cases radiotherapy alone may be performed (70 grays). Sarcomas (fibroblastic or Malignant fibrous histiocytoma) may occur after radiotherapy or without it. Hematogenous metastasis occur in 10% to 15% of patients. Survival rate at five years is included between 50% and 75%. Chondroid chordoma is a special entity occurring in younger patients (35 year old) and located in spheno-occipital region. In addition to chordomas it contain chondroid (benign or malignant) islands. Mean survival rate (16 years) is far better than for chordoma or chondrosarcoma.
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PMID:[Chordomas]. 329 77

Vimentin-positive, desmin-negative cells were established in culture from the nodule and from apparently normal palmar aponeurosis of a patient with Dupuytren's disease and compared with normal human embryonic and adult fibroblasts or sarcomatous cells. Cells from the nodule display in vitro biological properties that are intermediate between those expressed by normal fibroblasts and sarcoma cells or cells from the nodule transformed with SV40 virus. Thus, they represent an interesting in vitro model of partially transformed human cells. This behavior is not evolutive and justifies the classification of Dupuytren's disease among the benign mesenchymal tumors. The production of high level of plasminogen activator probably explains the local reactive pathology, and could act as a mitogenic stimulus for the proliferation of the nodule itself. Cultures derived from the apparently normal palmar aponeurosis show some but not all the abnormal growth properties of cells from nodules; this may help to explain the onset of local recurrences. Our results suggest that Dupuytren's disease is not strictly local and limited to the nodules, but affects, at least partially, the whole aponeurosis. Dupuytren's nodules could be considered as a model of tumor progression in a benign situation.
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PMID:Abnormal behavior of cultured fibroblasts from nodule and nonaffected aponeurosis of Dupuytren's disease. 619 20


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