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)

Metastatic clones growing in 0.6% 'hard' agar were selected from the non-metastatic Rous sarcoma virus (RSV)-transformed tumorigenic B77-3T3 mouse fibroblast line. The incidence of spontaneous lung metastases varied among clones around 100%, while it was lower than 5% in the parental tumor line. The organization of microfilaments, microtubules and intermediate filaments as well as the pattern of extracellular fibronectin matrix were analyzed by immunofluorescence in two representative clones (B77-AA6 and B77-AA12) and was compared with the structural features displayed by a highly metastasizing RSV-induced mouse sarcoma line (SR-BALB). In the metastatic clones studied microtubules and intermediate filaments were similarly organized in a pattern not significantly different from that of the non-metastatic parental cell line. The major finding was a marked concentration of actin-containing structures in the periphery of cells and notably at the level of surface protrusions, suggesting a high surface motility. In the same lines the production of fibronectin and its distribution in the cell layer and culture medium were analyzed. Metabolic labelling and immunofluorescence experiments indicated that the nonmetastasizing cells (B77-3T3) retain higher amounts of fibronectin in the cell layer and organize this molecule in extracellular fibers, while the metastatic clones (B77-AA6 and B77-AA12) as well as the metastatic line (SR-BALB) are unable to retain and organize fibronectin at their surface. This paper shows that the progression of tumorigenic cell lines toward a metastatic phenotype involves a redistribution of cytoskeletal actin and a loss of organized fibronectin matrix.
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PMID:Organization of cytoskeleton and fibronectin matrix in Rous sarcoma virus (RSV)-transformed fibroblast lines with different metastatic potential. 298 23

Certain tumour cells contain activated ras genes that code for 21 000 dalton proteins (p21). These proteins associate with the inner face of the plasma membrane and bind guanine nucleotides specifically. In order to determine whether p21s have functions similar to other GTP binding proteins, we investigated the regulation, by guanine nucleotides, of adenylate cyclase (AC) activity in membrane preparations isolated from fibroblasts (C127) transformed by a temperature sensitive mutant of Kirsten sarcoma virus (Ts 371). The degree of AC stimulation by GMP P(NH)P increased when these cells were shifted from the permissive temperature (33 degrees C) to the non-permissive temperature (39 degrees C). This effect was more pronounced at low Mg++ and low GMP P(NH)P concentrations. AC stimulation remained unchanged in rat fibroblasts infected with a temperature sensitive mutant of Rous Sarcoma virus. AC activity was depressed in C127 cells infected with wild type KiMSV. Our data illustrate the feasibility of correlating alterations in the AC system with ras gene expression and using such experimental approaches to elucidate the physiological functions of the p21 proteins.
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PMID:Modulation of adenylate cyclase by guanine nucleotides and Kirsten sarcoma virus mediated transformation. 298 13

Acquired immune deficiency syndrome (AIDS) can be transferred to patients by blood transfusions or human blood preparations, such as cryoprecipitates or factor VIII concentrates. Retroviruses have been discussed as infectious AIDS agents and more recently human T-lymphotropic retroviruses designated as HTLV type III and LAV (lymphadenopathy-associated virus) have been isolated from AIDS patients. Whether heat treatment at 60 degrees C (pasteurization) of liquid human plasma protein preparations inactivates retroviruses was therefore investigated. Pasteurization had already been included in the routine manufacturing process of human plasma protein preparations in order to guarantee safety with regard to hepatitis B. Since high titer preparations of human retroviruses were not available, heat inactivation was studied using Rous sarcoma virus added to the various plasma protein preparations tested. This retrovirus which was obtained in preparations of 6.0 log10 FFU/ml was shown to be at least as heat stable as two mammalian retroviruses studied, i.e., feline and simian sarcoma virus. In all of eight different plasma protein preparations tested, Rous sarcoma virus was completely inactivated after a heat treatment lasting no longer than 4 hr. It is thus concluded that pasteurization of liquid plasma protein preparations at 60 degrees C over a period of 10 hr must confer safety to these products with respect to AIDS, provided that the AIDS agents are retroviruses of comparable heat stability as Rous sarcoma virus and the mammalian retroviruses tested.
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PMID:Safety of human blood products: inactivation of retroviruses by heat treatment at 60 degrees C. 298 90

Computer based sequence comparisons indicate partial sequence homology between human c-myc, Rous sarcoma virus, adenovirus 7, and simian sarcoma virus proteins and the cytoskeletal proteins d9smin, keratin and vimentin. In addition, sections of the oncogene proteins showed partial but significant homology to alpha and gamma subunits of transducin. gamma-II and beta-BP crystallins showed partial but significant homology to the cytoskeletal proteins keratin, vimentin, desmin, alpha and beta-tubulin, and to adenovirus 7 and simian sarcoma virus transforming gene proteins. Beta-BP crystallin showed partial but significant homology to Rous sarcoma virus protein, and to alpha and gamma subunits of transducin. Both crystallins showed partial sequence homology to the GTP-binding protein elongation factor TU from Escherichia coli. These sequence homologies suggest a link between the mechanisms of normal lens cell differentiation, involving modifications to the cytoskeleton and subsequent changes to the pattern of protein synthesis, and mechanisms of neoplastic transformation. Furthermore, the transducin-like region on beta-crystallin may be important for its interaction with lens membranes and the maintenance of short-range order for lens transparency.
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PMID:Partial sequence homologies between cytoskeletal proteins, c-myc, Rous sarcoma virus and adenovirus proteins, transducin, and beta- and gamma-crystallins. 298 44

Immunization with mouse and rat cells transformed by Rous sarcoma virus (RSV) or by B77 avian sarcoma virus (ASV) induced complete transplantation resistance against an RSV-induced mouse tumor (CSA1M) in syngeneic hosts. In contrast, most of the mice immunized with a Fujinami sarcoma virus-transformed rat fibroblast line (FSV-3Y1), a feline sarcoma virus-transformed cat fibroblast line (FeSV-FEF), an Abelson leukemia virus-infected Balb/3T3 cell line (AbLV-3T3), or an uninfected 3Y1 cell line could not reject the CSA1M. Serologic analysis with the use of a complement-dependent cytotoxicity assay supported the results of transplantation studies. The mouse and rat cells transformed by RSV or B77 ASV expressed a common tumor-specific cell surface antigen (TSSA) detected by syngeneic antiserum against the CSA1M, whereas none of the FSV-3Y1, FeSV-FEF, and AbLV-3T3 cells expressed the TSSA. These results suggest that the common TSSA in the mouse and rat cells transformed by RSV or B77 ASV containing src gene is not shared with mammalian cells infected with retroviruses transducing other oncogenes of the src gene family (i.e., fps, fes, and abl).
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PMID:No expression of a Rous sarcoma virus-induced tumor antigen in mammalian cells infected with retroviruses transducing other oncogenes of the src gene family. 298 59

Several chimeric murine retroviruses were constructed to test whether the gag sequence of Abelson murine leukemia virus (A-MuLV) could influence the in vitro specificity of two sarcoma-inducing oncogenes: src of Rous sarcoma virus and fps of Fujinami sarcoma virus. Although the src- or fps- containing chimerae could transform fibroblasts, they were unable to mimic the action of A-MuLV in causing lymphoid transformation in vitro. A-MuLV-derived gag sequences could, however, functionally replace the 5' end of src and restore the transformation potential of a 5'-truncated src gene. To investigate this functional similarity, we replaced the gag sequence of an A-MuLV virus with the 5' end of src. This recombinant virus behaved like the A-MuLV virus from which it was derived: it transformed both fibroblasts and lymphoid cells in vitro. Taken together, these results suggest that lymphoid transformation in vitro is a specific property of abl and not of src or fps. Furthermore, it shows that a functional homology exists between the gag sequence of A-MuLV and the 5' end of src.
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PMID:Specific transforming potential of oncogenes encoding protein-tyrosine kinases. 299 40

A brain-tumor model in adult monkeys may be significant because of the biological similarity to humans as well as the feasibility for surgical manipulation and for sequential computerized tomography (CT) scanning. In the present study, brain tumors were successfully produced in Japanese monkeys (Macaca fuscata), each weighing 2 to 10.8 kg, with an average age of 5.1 years old. Tumor cells were implanted by intracerebral inoculation of 4 X 10(7) chick embryo fibroblasts infected with the Schmidt-Ruppin strain of Rous sarcoma virus (RSV). With a 15- to 67-day latency, brain tumors were induced in 11 (73.3%) of 15 RSV-inoculated monkeys. Contrast-enhanced CT scans delineated all solitary intracerebral tumors greater than 4 to 6 mm in diameter. The CT images were proved at autopsy to be accurate within 2 mm in determining the size of tumor. Five of the 11 monkeys with intracerebral tumors died, with an average survival time of 26.6 days after RSV inoculation. The induced tumors were classified as either glioma or sarcoma by the presence or absence of glial fibrillary acidic protein (GFAP) and S-100 protein. A chromosome analysis of cultured tumor cells showed a diploid number of 42, indicating monkey origin. It is concluded that the reproducible brain tumor in the adult Japanese monkey inoculated with RSV can serve as a good experimental brain-tumor model for the further study of human malignant brain tumors.
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PMID:Establishment of a brain-tumor model in adult monkeys. 299 16

Five individual male matings of line UNH 105 New Hampshires, in which all males and most females were either B22/B24 or B22/B26, produced 462 progeny that fell into six B complex genotypes: B22/B22, B24/B24, B26/B26, B22/B24, B22/B26, and B24/B26. The genotypes of parents and offspring were determined by blood typing for B alloantigens using a panel of antisera. Six-week-old chickens were inoculated with Rous sarcoma virus (RSV). Resulting tumors were scored for size six times over a 10-week period; based upon these scores, a tumor profile index (TPI) was assigned to each chicken as a criterion of immunological response. The B22/B26 hosts showed the greatest mean response (TPI 3.3) and B24/B24 chickens the lowest response (TPI 4.4), the difference being statistically significant. Dominance in the response to sarcoma was observed when either the B22 or B26 haplotype combined with the B24 haplotype and compared with the appropriate corresponding homozygotes, and when the B22 or B26 heterozygote was compared with B22/B22 and B26/B26 homozygotes.
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PMID:Response of B complex haplotypes B22, B24, and B26 to Rous sarcomas. 299 42

The development of histocompatible White Leghorn (progressor) and Arkansas Regression (regressor) chicken lines was described. When challenged with Rous sarcoma virus, progressor chickens developed fatal tumors while the regressor chickens eliminated the sarcoma. When sensitized histocompatible peritoneal macrophages and blood lymphocytes were transferred from regressor donors to progressor recipients, they both eradicated growing tumors. Histoincompatible cells were ineffective in inducing tumor remission. Within the two age groups tested, the sensitized blood lymphocytes and macrophages were only effective when transferred between age-matched donor and recipient chickens.
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PMID:Transfer of blood lymphocytes and macrophages between histocompatible progressor and regressor chickens infected with Rous sarcoma virus. 301 78

The mechanism of cellular src (c-src) transduction by a transformation-defective deletion mutant, td109, of Rous sarcoma virus was studied by sequence analysis of the recombinational junctions in three td109-derived recovered sarcoma viruses (rASVs). Our results show that two rASVs have been generated by recombination between td109 and c-src at the region between exons 1 and 2 defined previously. Significant homology between td109 and c-src sequences was present at the sites of recombination. The viral and c-src sequence junction of the third rASV was formed by splicing a cryptic donor site at the 5' region of env of td109 to exon 1 of c-src. Various lengths of c-src internal intron 1 sequences were incorporated into all three rASV genomes, which resulted from activation of potential splice donor and acceptor sites. The incorporated intron 1 sequences were absent in the c-src mRNA, excluding its being the precursor for recombination with td109 and implying that initial recombinations most likely took place at the DNA level. A potential splice acceptor site within the incorporated intron 1 sequences in two rASVs was activated and was used for the src mRNA synthesis in infected cells. The normal env mRNA splice acceptor site was used for src mRNA synthesis for the third rASV.
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PMID:Transduction of c-src coding and intron sequences by a transformation-defective deletion mutant of Rous sarcoma virus. 301 20


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