Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.21.4 (trypsin)
 42,187 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Numerical and structural chromosome analysis of a human retroperitoneal liposarcoma cell line maintained under standard cell culture conditions revealed a very stable hypodiploid mode. If the cells were not trypsinized for several generations, a near-triploid stemline, which was generally a duplication of the hypodiploid mode, emerged. Some chromosomes appeared to be relatively stable pairs (1, 2, 7, 9, and 12), but most had "lost" one homolog or both (4 and 21) or were rearranged into "new" marker chromosomes. Quantitation of the genetic material showed a loss of 12.0 +/- 3.7% per spread. Only one characteristically long marker chromosome, which is present in every cell, could be identified with certainty as a translocation between chromosomes 4 and 11. Several of the marker chromosomes showed interstitial negatively staining regions with the trypsin-Giemsa method.
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PMID:Chromosome studies on a human liposarcoma cell line. 47 12

A chromosomal study was used to establish diagnosis of a poorly differentiated soft-tissue sarcoma occurring in the right thigh of a 57-year-old Japanese female. Histopathologically the excised tumor consisted of a poorly differentiated myxoid neoplasm, without specific features to enable the identification of neoplastic cells. Although a tentative diagnosis of poorly differentiated myxoid liposarcoma was made, ultrastructural examination and Oil Red O fat stain failed to demonstrate the evidence of lipoblastic differentiation, except that occasional cells possessed a small number of fine fat droplets. The diagnosis of liposarcoma was suggested by chromosome analysis of the fresh tumor tissue after short time culture and trypsin-Giemsa banding technique. The tumor cells demonstrated a clonal abnormality characterized by a reciprocal translocation, t(12; 16)(q 13; p 11), which is known as a specific aberration in myxoid liposarcoma. Thus, chromosome study seems to be useful for identifying undifferentiated mesenchymal tumors, which lack morphologic evidence of any specific differentiation, as in the present case.
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PMID:Myxoid liposarcoma with t (12; 16)(q 13; p 11). Possible usefulness of chromosome analysis in a poorly differentiated sarcoma. 143 36

A murine monoclonal antibody (E10) was made against cultured cartilage cells. The E10 antibody binding is localized to the surface of cultured cartilage cells in suspension and is present in the cytoplasm in paraffin embedded sections. There is no reactivity with cartilage matrix, or with the matrix of cartilaginous tumors. Reactivity is removed by treatment with trypsin and hyaluronidase, but not by treatment with heparinase, neuraminidase, and chondroitinase. Regeneration of E10 antigen after trypsinization takes 48 hours in chondrocytes in tissue culture. SDS-polyacrylamide gel electrophoresis of an E10 immune precipitate of cultured chondrocytes results in two peaks: one at a very high molecular weight and a small fragment at approximately 250 kd. Specificity has been demonstrated by cytofluorometry, immunofluorescence, and immunohistochemistry, in both frozen and paraffin-embedded tissues. Positive reactivity was seen in cultured cartilage cells, chondrocytes in fetal and adult cartilage, chondrosarcomas, and chordomas. Minimal reactivity was found in a chondromyxoid liposarcoma. Acinar cells of salivary and sweat glands and mast cells in various tissues and tumors were also positive. There was no reactivity with other tissues and tumors, including myxoid and mucinous tumors and epithelial tissues.
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PMID:Monoclonal antibody to human cartilage cells and its reactivities to chondrocytic tumors. 206 41