Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0029463 (osteosarcoma)
 16,637 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Proto-oncogene fos is a multifaceted gene, which is expressed during cell growth, cell differentiation, and development. The viral homologue, v-fos, was identified as the resident transforming gene of FBJ-murine osteosarcoma virus which induces bone tumors in mice. Due to an in-fram deletion during the biogenesis of the v-fos gene, the products of viral and cellular fos proteins differ at their C-termini. Despite different C-termini, both fas proteins are nuclear in their location, and can transform fibroblasts in vitro. However, transformation by c-fos gene requires removal of a 67 base pair sequence from the 3' non-coding domain. Proto-oncogene fos is a highly inducible gene in response to a variety of growth factors and differentiation-specific inducers. The transcriptional enhancer and the inducible element of the fos gene have been mapped along with sequences in the 3' non-coding domain which may influence the stability of the c-fos transcripts. The c-fos gene transcription is regulated by positively and negatively acting cellular factors.
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PMID:Proto-oncogene fos: an inducible gene. 333 16

The expression of 7 protooncogenes (c-sis, c-abl, c-mos, c-bas, c-Ki-ras, c-fos, c-myc) was examined in transplants and established cell lines from spontaneous and radiation-induced murine osteosarcomas. The transplant tumors were compared with different tissues, particularly skeletal tissue (sternum), and the osteosarcoma cell lines with fibroblast lines from the same mouse strains. C-sis was expressed above the level of controls in 2 osteosarcomas (TV, Os5). Three osteosarcomas showed over-expression of c-abl (TVK, DOS, Os5), c-bas (DOS, Os5 and V893) and c-fos (TVK, DOS, Os5), and 4 osteosarcomas showed over-expression of c-Ki-ras (TVK, DOS, Os5, Os16) and c-myc (TVK, DOS, TV, Os5). C-mos expression was not observed under the conditions used. One cell line (Os5) showed an altered transcript (1 kb transcript of c-fos). Apart from the relatively frequent increase in expression of the c-myc and c-ras-family, there was no indication that any particular protooncogene or combination of protooncogenes was associated with murine osteosarcomas.
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PMID:Expression of protooncogenes in murine osteosarcomas. 345 17

Regulation of transcription in eukaryotes is mediated by the specific interaction between cellular factors and promoter sequences. Cis-acting DNA sequences, frequently located upstream of the TATA box, have been implicated in modulating the expression of many genes. We are interested in the transcriptional regulation of proto-oncogenes because they may have a pivotal function in cell growth and differentiation. Expression of the proto-oncogene c-fos is induced in response to a variety of growth factors and differentiation-specific agents. The viral cognate of the c-fos gene is the resident transforming gene of FBJ-murine osteosarcoma virus which causes bone tumours in vivo and cellular transformation in vitro. We report here that transcription of the human c-fos gene is modulated by negatively and positively acting cellular factors.
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PMID:Modulation of c-fos gene transcription by negative and positive cellular factors. 356 89

The transforming gene of the osteosarcoma-producing FBJ murine sarcoma virus, v-fos, is homologous to a normal cellular gene, c-fos, in vertebrate species. Transcripts from the c-fos proto-oncogene accumulate to very high levels in late gestational mouse and human extra-embryonic tissues. We now report that these RNA transcripts are translated in these tissues. Rabbits were immunized with a synthetic peptide whose sequence is common to both c-fos and v-fos. After affinity purification on an immunosorbent containing the fos peptide (a nonapeptide), the antibody reacted with a component(s) in nuclei in sections of human and murine tissues and immunoprecipitated the v-fos gene product (p55) and a cellular protein of 39 kd (p39, complexed with fos) from lysates of metabolically-labelled virally transformed cells. Crude extracts of normal tissues contained major anti-fos-reactive proteins in the range of 55-60 kd as shown by protein blot analysis. Indirect immunofluorescence and immunoperoxidase staining showed that in addition to strong immunoreactive component(s) in the nuclei of extra-embryonic tissues of human and mouse, weaker reactions are detectable in all normal fetal and adult tissues tested. This demonstrates that fos-reactive protein is expressed in a wide variety of cells and tissues.
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PMID:Product of the cellular oncogene, c-fos, observed in mouse and human tissues using an antibody to a synthetic peptide. 389 12

The human cellular homolog (c-fos) of the transforming gene of Finkel-Biskis-Jinkins (FBJ) murine osteosarcoma virus was mapped to a single human chromosome. DNA from a series of 31 mouse-human somatic cell hybrid lines was probed with v- and c-fos molecular clones by Southern blotting. Human c-fos segregated with the distal region of the long arm of human chromosome 14. In situ hybridization of 125I-labeled human c-fos probe to normal human metaphase chromosomes independently confirmed these results and localized the c-fos oncogene to region 14q21----q31.
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PMID:Human c-fos oncogene mapped within chromosomal region 14q21----q31. 609 Nov 12

The 8.2-kilobase (kb) unintegrated circular DNA form of the FBJ murine leukemia virus (FBJ-MLV) was linearized by cleavage at the single HindIII site, molecularly cloned into bacteriophage Charon 30, and subsequently subcloned into pBR322 (pFBJ-MLV-1). Both FBJ-MLV virion RNA and pFBJ-MLV-1 DNA were used to investigate the arrangement of helper virus sequences in the FBJ murine osteosarcoma virus genome (FBJ-MSV) by heteroduplex formation with cloned FBJ-MSV proviral DNA. The results showed that the FBJ-MSV genome contained 0.8 kb of helper virus sequence at its 5' terminus and 0.98 kb at its 3' terminus. Approximately 6.8 kb of helper virus sequence had been deleted, and 1.7 kb of unrelated sequence was inserted into the FBJ-MSV genome. This substituted region contains v-fos, the transforming gene of FBJ-MSV. Using a probe specific for v-fos, we have cloned homologous sequences (c-fos) from mouse and human chromosomal DNA. Heteroduplex analysis of FBJ-MSV DNA with these recombinant clones showed that both the c-fos(mouse) and the c-fos(human) sequences hybridized to the entire 1.7-kb v-fos region. However, five regions of homology of 0.27, 0.26, 0.14, 0.5, and 0.5 kb were separated by four regions of nonhomology of 0.76, 0.55, 0.1, and 0.1 kb from 5' to 3' with respect to the FBJ-MSV genome. The size of these sequences showed striking similarity in both c-fos(mouse) and c-fos(human).
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PMID:Structure of the FBJ murine osteosarcoma virus genome: molecular cloning of its associated helper virus and the cellular homolog of the v-fos gene from mouse and human cells. 630 48

The FBJ murine osteosarcoma virus (FBJ-MuSV) induces osteosarcomas in mice and transforms fibroblasts in vitro. It contains an oncogene termed v-fos derived from a normal cellular gene by recombination with an associated helper virus. The product of the v-fos gene is a 55,000 dalton protein, p55v-fos. This protein was found in the nuclei of cells containing amplified levels of the v-fos gene, and also in the nuclei of virus-transformed cells. The c-fos protein was localized in the nuclei of normal mouse amnion cells and in the nuclei of cells transformed by a recombinant plasmid that expresses the c-fos gene product. However, p55c-fos undergoes more extensive post-translational modification in the nucleus than p55v-fos. Immunofluorescence data indicate that the level of p55c-fos in normal mouse amnion cells is similar to that found in fibroblasts transformed by the v-fos or c-fos proteins.
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PMID:Viral and cellular fos proteins: a comparative analysis. 631 13

The FBR murine osteosarcoma virus complex, isolated from a radiation-induced osteosarcoma of an X/Gf mouse causes the rapid appearance of osteosarcomas in newborn mice and transforms fibroblasts in vitro. The two components of the FBR-viral complex have been isolated separately in tissue culture: FBR-MuLV by end-point dilution and FBR-MuSV by the establishment of mouse [FBR-NP 117 (NIH 3T3)] and rat non-producer cell lines [FBR-NP415 (REF)]. The host range and RNase Tl fingerprint analysis of FBR-MuLV demonstrated a pattern closely related to, but distinguishable from, Akv-MuLV. Transformed cells from both mice and rats contain a rescuable FBR-MuSV genome. These pseudotypes produce foci in tissue culture and induce osteosarcomas in susceptible mouse strains. An FBR-MuSV (FBR-MuLV) cDNA probe detects a 5.2 kb HindIII and a 9.5 kb EcoRI FBR-MuSV-specific fragment in FBR-MuSV-transformed non-producer rat cells. The same fragments hybridized with a fos specific probe, demonstrating that FBR-provirus contains a c-fos-derived onc-gene.
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PMID:Characterization of the FBR-murine osteosarcoma virus complex: FBR-MuSV encodes a FOS-derived oncogene. 632 27

The complete nucleotide sequence of the c-fos(human) gene, the human cellular homolog of the oncogene (v-fos) of Finkel-Biskis-Jinkins murine osteosarcoma virus, has been determined. The c-fos(human) gene contains four discontinuous regions when compared with the v-fos gene. Three of the discontinuities are flanked by sequences characteristic of introns, while the fourth discontinuity is due to a deletion of 104 base pairs in the v-fos gene. As a consequence of the deletion, the predicted c-fos(human) and v-fos gene products differ at their carboxyl termini. Transcripts of 2.2 kilobases from the c-fos(human) gene have been identified in human cells. The sizes of these transcripts are in close agreement with the size expected from the nucleotide sequence after removal of introns.
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PMID:Complete nucleotide sequence of a human c-onc gene: deduced amino acid sequence of the human c-fos protein. 657 79

The FBJ murine osteosarcoma virus (FBJ-MuSV) induces tumors in vivo and transformation in vitro. Transformation is due to the expression of a single viral protein (p55v-fos) which is encoded by sequences derived from mouse genetic material. The homologous cellular gene (c-fos) does not transform cultured cells after introduction by transfection. We show that even though the c-fos protein is completely different from the v-fos protein at its C terminus, it is capable of transforming cultured fibroblasts. However, activation of the transforming potential of the c-fos gene requires two manipulations--a transcriptional enhancer sequence must be linked to the gene and an interaction at the 3' end of the gene, which inhibits transformation, must be disrupted. Our studies show that normal cellular protein can induce transformation when expressed in an inappropriate cell type.
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PMID:c-fos protein can induce cellular transformation: a novel mechanism of activation of a cellular oncogene. 660 18


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