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  • *Oncogenes  (8)
  • American Association for the Advancement of Science (AAAS)  (8)
  • American Chemical Society
  • American Geophysical Union
  • Springer
  • 1980-1984  (8)
  • 1984  (8)
Collection
Keywords
Publisher
  • American Association for the Advancement of Science (AAAS)  (8)
  • American Chemical Society
  • American Geophysical Union
  • Springer
Years
  • 1980-1984  (8)
Year
  • 1
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    Autoimmunity and increased c-myb transcription (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-11-30
    Description: A single recessive gene, lpr, induces an autoimmune-lymphoproliferative syndrome in several strains of mice. The lymphoid organs of lpr/lpr mice contained cells with increased amounts of myb RNA, which codes for a protein found in the nucleus. A similar human lymphoproliferative disorder also had an increase in c-myb expression. Mouse T cells induced by mitogens to proliferate did not express large amounts of myb RNA, indicating that marked myb expression is not a general feature of lymphocyte activation and proliferation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mountz, J D -- Steinberg, A D -- Klinman, D M -- Smith, H R -- Mushinski, J F -- New York, N.Y. -- Science. 1984 Nov 30;226(4678):1087-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6494925" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autoantibodies/*genetics ; Autoimmune Diseases/*genetics ; Female ; *Genes, Recessive ; Lymphocytes/immunology ; Lymphoproliferative Disorders/*genetics ; Mice ; Mice, Inbred Strains ; Nucleic Acid Hybridization ; *Oncogenes ; Species Specificity ; Spleen/immunology ; *Transcription, Genetic
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    Detection of c-sis transcripts and synthesis of PDGF-like proteins by human osteosarcoma cells (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-11-23
    Description: Platelet-derived growth factor (PDGF) has been previously shown to be homologous to the transforming gene of simian sarcoma virus (v-sis), and inappropriate expression of the cellular counterpart of the v-sis gene (c-sis) has been implicated in the generation of mesenchymal tumors. The U-2 OS human osteosarcoma line was shown to contain multiple c-sis transcripts. Immunoprecipitation experiments with antiserum to PDGF identified a variety of polypeptides ranging in size from 18,000 to 165,000 daltons that were immunoprecipitated specifically from U-2 OS cell extracts. The osteosarcoma also was shown to secrete a 29,000-dalton protein having the serological and structural characteristics of PDGF.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Graves, D T -- Owen, A J -- Barth, R K -- Tempst, P -- Winoto, A -- Fors, L -- Hood, L E -- Antoniades, H N -- CA30101/CA/NCI NIH HHS/ -- HL27607/HL/NHLBI NIH HHS/ -- HL29583/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1984 Nov 23;226(4677):972-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6209798" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; DNA Replication ; Humans ; Molecular Weight ; Neoplasm Proteins/*genetics ; *Oncogenes ; Osteosarcoma/*genetics ; *Platelet-Derived Growth Factor ; Poly A/genetics/isolation & purification ; RNA/genetics/isolation & purification ; RNA, Messenger ; *Transcription, Genetic
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    Repression of rearranged mu gene and translocated c-myc in mouse 3T3 cells X Burkitt lymphoma cell hybrids (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-04-27
    Description: The productively rearranged immunoglobulin mu chain gene and the translocated cellular oncogene c-myc are transcribed at high levels both in human Burkitt lymphoma cells carrying the t(8;14) chromosome translocation and in mouse plasmacytoma X Burkitt lymphoma cell hybrids. In the experiments reported here these genes were found to be repressed in mouse 3T3 fibroblast X Burkitt lymphoma cell hybrids. Such repression probably occurs at the transcriptional level since no human mu- and c-myc messenger RNA's are detectable in hybrid clones carrying the corresponding genes. It is therefore concluded that the ability to express these genes requires a differential B cell environment. The results suggest that the 3T3 cell assay may not be suitable to detect oncogenes directly involved in human B cell oncogenesis, since 3T3 cells apparently are incapable of transcribing an oncogene that is highly active in malignant B cells with specific chromosomal translocations.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nishikura, K -- ar-Rushdi, A -- Erikson, J -- DeJesus, E -- Dugan, D -- Croce, C M -- CA 09171/CA/NCI NIH HHS/ -- CA 10815/CA/NCI NIH HHS/ -- GM 31060/GM/NIGMS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1984 Apr 27;224(4647):399-402.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6424234" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Burkitt Lymphoma/*genetics ; Fibroblasts ; *Gene Expression Regulation ; Genes ; Humans ; Hybrid Cells/*metabolism ; Immunoglobulin Heavy Chains/*genetics ; Immunoglobulin mu-Chains/*genetics ; Mice ; *Oncogenes ; RNA, Messenger/genetics ; Transcription, Genetic ; *Translocation, Genetic
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
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    Sequencing the erbA gene of avian erythroblastosis virus reveals a new type of oncogene (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-06-29
    Description: Avian erythroblastosis virus (AEV) contains two distinct oncogenes, erbA and erbB . The erbB oncogene, which is homologous to a portion of the epidermal growth factor receptor, is related to the src family of oncogenes and efficiently transforms erythroblasts, whereas erbA potentiates the effects of erbB by blocking the differentiation of erythroblasts at an immature stage. This "potentiator" was sequenced; the amino acid sequence deduced from it was clearly different from the sequences of other known oncogene products and was related to carbonic anhydrases. These enzymes participate in the transport of carbon dioxide by erythrocytes, the precursors of which are main targets of avian erythroblastosis virus. A src-related oncogene such as erbB in synergy with an activated specific cell-derived gene such as erbA can profoundly affect early erythroid differentiation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Debuire, B -- Henry, C -- Bernissa, M -- Biserte, G -- Claverie, J M -- Saule, S -- Martin, P -- Stehelin, D -- New York, N.Y. -- Science. 1984 Jun 29;224(4656):1456-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6328658" target="_blank"〉PubMed〈/a〉
    Keywords: Alpharetrovirus/*genetics ; Avian Leukosis Virus/*genetics ; Avian Sarcoma Viruses/genetics ; Base Sequence ; Carbonic Anhydrases/genetics ; DNA, Viral/genetics ; Erythropoiesis ; Humans ; *Oncogenes
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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    Requirement for a signal sequence in biological expression of the v-sis oncogene (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-12-07
    Description: The protein encoded by the simian sarcoma virus oncogene (v-sis) contains a signal sequence, derived from the envelope gene of the parental retrovirus, which is required for transformation. Removal of the proposed signal sequence was correlated with loss of biological activity. This activity was restored to inactive deletion mutants by fusion with the coding region for a heterologous signal sequence. Biological activity of v-sis was also abolished by either a small deletion within the coding region of the signal sequence or by a point mutation introduced by site-directed mutagenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hannink, M -- Donoghue, D J -- CA34456/CA/NCI NIH HHS/ -- GM07313/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1984 Dec 7;226(4679):1197-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6095451" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Transformation, Viral ; *Gene Expression Regulation ; Mutation ; *Oncogenes ; *Protein Biosynthesis ; Retroviridae/*genetics ; Sarcoma Virus, Woolly Monkey/*genetics ; Viral Proteins/biosynthesis
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
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    Amplification of the c-myb oncogene in a case of human acute myelogenous leukemia (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-06-08
    Description: Amplification is one of the mechanisms by which cellular oncogenes may be altered in their function, possibly leading to neoplastic transformation. The oncogenes c-myc, c- abl , and c-Ki-ras are amplified in several different human neoplasias. The oncogene c-myb, which is specifically expressed and regulated in hematopoietic cells, was found to be amplified in cell lines ML-1, ML-2, and ML-3, which were separately cultured from cells of a patient with acute myelogenous leukemia (AML). A five- to tenfold amplification was correlated with high levels of expression of normal size c-myb messenger RNA and with chromosomal abnormalities in the region 6q22 -24, where the c-myb locus is normally located. Amplification and cytogenetic abnormalities were detected in DNA's from primary and secondary cultures of ML cells, suggesting that they may have contributed to leukemogenesis. The similar AML cell lines HL-60 and ML's contain different amplified oncogenes: c-myc and c-myb, respectively. Alternative activation of structurally and possibly functionally similar oncogenes may distinguish--at the pathogenetic level--phenotypically similar tumors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pelicci, P G -- Lanfrancone, L -- Brathwaite, M D -- Wolman, S R -- Dalla-Favera, R -- P30 CA-16087/CA/NCI NIH HHS/ -- RR 05399/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 1984 Jun 8;224(4653):1117-21.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6585957" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; DNA, Neoplasm/genetics ; *Gene Amplification ; Humans ; Karyotyping ; Leukemia, Myeloid, Acute/*genetics ; Nucleic Acid Hybridization ; *Oncogenes
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
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    Expression of cellular oncogenes in human malignancies (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-04-20
    Description: Cellular oncogenes have been implicated in the induction of malignant transformation in some model systems in vitro and may be related to malignancies in vivo in some vertebrate species. This article describes a study of the expression of 15 cellular oncogenes in fresh human tumors from 54 patients, representing 20 different tumor types. More than one cellular oncogene was transcriptionally active in all of the tumors examined. In 14 patients it was possible to study normal and malignant tissue from the same organ. In many of these patients, the transcriptional activity of certain oncogenes was greater in the malignant than the normal tissue. The cellular fes (feline sarcoma) oncogene, not previously known to be transcribed in mammalian tissue, was found to be active in lung and hematopoietic malignancies.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Slamon, D J -- deKernion, J B -- Verma, I M -- Cline, M J -- AM 18058/AM/NIADDK NIH HHS/ -- CA 15619/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1984 Apr 20;224(4646):256-62.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6538699" target="_blank"〉PubMed〈/a〉
    Keywords: Adenocarcinoma/genetics ; Breast Neoplasms/genetics ; Carcinogens/pharmacology ; Cell Differentiation ; Cell Division ; Cell Transformation, Neoplastic ; Female ; Gastrointestinal Neoplasms/genetics ; Gene Amplification ; Genes, Viral ; Genital Neoplasms, Female/genetics ; Humans ; Kidney Neoplasms/genetics ; Leukemia/genetics ; Lymphoma/genetics ; Methylation ; Mutation ; Neoplasms/*genetics ; Nucleic Acid Hybridization ; *Oncogenes ; RNA, Messenger/genetics ; RNA, Neoplasm/genetics ; Sarcoma/genetics ; *Transcription, Genetic ; Translocation, Genetic
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 8
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    Malignant activation of a K-ras oncogene in lung carcinoma but not in normal tissue of the same patient (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-02-17
    Description: A single genetic alteration, a guanine-to-cytosine transversion, is responsible for the acquisition of malignant properties by K-ras genes of two human tumor cell lines established from carcinomas of the bladder (A1698) and lung (A2182). As a consequence, arginine instead of the normal glycine is incorporated into the K-ras-coded p21 proteins at amino acid position 12. This mutation creates a restriction enzyme polymorphism that can be used to screen human cells for transforming K-ras genes. This approach was used to identify the mutational event responsible for the malignant activation of a K-ras oncogene in a squamous cell lung carcinoma of a 66-year-old man; this point mutation was not present in either the normal bronchial or parenchymal tissue or in the blood lymphocytes. Hence, malignant activation of a ras oncogene appears to be specifically associated with the development of a human neoplasm.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Santos, E -- Martin-Zanca, D -- Reddy, E P -- Pierotti, M A -- Della Porta, G -- Barbacid, M -- New York, N.Y. -- Science. 1984 Feb 17;223(4637):661-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6695174" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; *Cell Transformation, Neoplastic ; DNA, Neoplasm/genetics ; Genes, Dominant ; Humans ; Lung Neoplasms/*genetics ; Mutation ; *Oncogenes ; Organ Specificity ; Polymorphism, Genetic
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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