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  • *Oncogenes  (37)
  • American Association for the Advancement of Science (AAAS)  (37)
  • American Chemical Society
  • Annual Reviews
  • 1980-1984  (37)
  • 1984  (37)
Collection
Keywords
Publisher
  • American Association for the Advancement of Science (AAAS)  (37)
  • American Chemical Society
  • Annual Reviews
Years
  • 1980-1984  (37)
Year
  • 1
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    The human homologs of the raf (mil) oncogene are located on human chromosomes 3 and 4 (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-01-06
    Description: Two human genes that are homologous to both the murine transforming gene (oncogene) v-raf and the chicken transforming gene v-mil have been mapped by means of human-rodent somatic cell hybrids to human chromosomes previously devoid of known oncogenes. One gene, c-raf-2, which appears to be a processed pseudogene, is located on chromosome 4. The other gene, c-raf-1, which appears to be the active gene, is located on chromosome 3 and has been regionally mapped by chromosomal in situ hybridization to 3p25. This assignment correlates with specific chromosomal abnormalities associated with certain human malignancies.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bonner, T -- O'Brien, S J -- Nash, W G -- Rapp, U R -- Morton, C C -- Leder, P -- New York, N.Y. -- Science. 1984 Jan 6;223(4631):71-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6691137" target="_blank"〉PubMed〈/a〉
    Keywords: Adenocarcinoma/genetics ; Animals ; Chromosome Aberrations ; Chromosome Mapping ; *Chromosomes, Human, 1-3 ; *Chromosomes, Human, 4-5 ; Cricetinae ; Humans ; Hybrid Cells ; Kidney Neoplasms/genetics ; Lung Neoplasms/genetics ; Male ; Mice ; 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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  • 2
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    Altered transcription of the c-abl oncogene in K-562 and other chronic myelogenous leukemia cells (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-07-06
    Description: Expression of the cellular abl (c- abl ) oncogene was studied in K-562 and other chronic myelogenous leukemia (CML) cells and cell lines by means of Northern blot hybridization. In contrast to non-CML cells, which contained 7.4- and 6.8-kilobase abl -related transcripts, the CML cells contained a predominant and novel 8.2-kilobase abl -related RNA. In addition, the levels of abl -related message were up to eight times higher in CML cell lines from patients at the blast crisis stage of the disease compared with CML cells obtained during the chronic phase and with non-CML cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Collins, S J -- Kubonishi, I -- Miyoshi, I -- Groudine, M T -- New York, N.Y. -- Science. 1984 Jul 6;225(4657):72-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6587568" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Chromosomes, Human, 21-22 and Y ; Chromosomes, Human, 6-12 and X ; DNA, Neoplasm/genetics ; Humans ; Leukemia, Myeloid/*genetics ; Mice ; Nucleic Acid Hybridization ; *Oncogenes ; RNA, Messenger/genetics ; *Transcription, Genetic
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    Nucleotide sequence of a human Blym transforming gene activated in a Burkitt's lymphoma (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-08-03
    Description: The nucleotide sequence of a human Blym-1 transforming gene activated in a Burkitt's lymphoma cell line was determined. This sequence predicts a small protein of 58 amino acids that is 33 percent identical to the predicted product of chicken Blym-1, the activated transforming gene of chicken B cell lymphomas. Both the human and chicken Blym-1 genes exhibit significant identity to an amino-terminal region of transferrins.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Diamond, A -- Devine, J M -- Cooper, G M -- CA 07250/CA/NCI NIH HHS/ -- CA 28946/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1984 Aug 3;225(4661):516-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6330897" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Base Sequence ; Burkitt Lymphoma/*genetics ; Cell Line ; *Cell Transformation, Neoplastic ; DNA Restriction Enzymes ; Humans ; *Oncogenes ; Structure-Activity Relationship ; Transcription, Genetic ; Transferrin/genetics
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  • 4
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    Human-proto-oncogene nucleotide sequences corresponding to the transforming region of simian sarcoma virus (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-02-03
    Description: The nucleotide sequences of the six regions within the normal human cellular locus (c-sis) that correspond to the entire transforming region of the simian sarcoma virus (SSV) genome (v-sis) were determined. The regions are bounded by acceptor and donor splice sites and, except for region 6, resemble exons. Region 6 lacks a 3' donor splice site and terminates -5 base pairs from the 3' v-sis-helper-viral junction. This is consistent with a model proposing that SSV was generated by recombination between proviral DNA of a simian sarcoma associated virus and proto-sis and that introns were spliced out subsequently from a fused viral-sis messenger RNA. This also suggests that the 3' recombination occurred within an exon of the woolly monkey (Lagothrix) genome. The open reading frames predicting the v-sis and c-sis gene products coincide with the stop codon of c-sis located 123 nucleotides into the fifth region of homology. The overall nucleotide homology was 91 percent with substitutions mainly in the third codon positions within the open reading frame and with greatest divergence within the untranslated 3' portion of the sequences. The predicted protein products for v-sis and c-sis are 93 percent homologous. The predicted c-sis gene product is identical in 31 of 31 amino acids to one of the published sequences of platelet-derived growth factor. Thus, c-sis encodes one chain of human platelet-derived growth factor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Josephs, S F -- Guo, C -- Ratner, L -- Wong-Staal, F -- New York, N.Y. -- Science. 1984 Feb 3;223(4635):487-91.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6318322" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Base Sequence ; Cell Transformation, Neoplastic ; Cell Transformation, Viral ; Codon ; *Genes, Viral ; Humans ; *Oncogenes ; Platelet-Derived Growth Factor/*genetics ; RNA Splicing ; RNA, Messenger/genetics ; Recombination, Genetic ; Retroviridae/*genetics ; Sarcoma Virus, Woolly Monkey/*genetics ; Viral Proteins/genetics
    Print ISSN: 0036-8075
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  • 5
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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
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  • 6
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    Activated expression of the N-myc gene in human neuroblastomas and related tumors (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-12-14
    Description: In neuroblastoma lines in which the N-myc gene is present as a single copy, the expression of N-myc as messenger RNA is increased relative to that in nonneuroblastoma cell lines and tumors. The increase of expression in neuroblastomas with amplified N-myc genes is the result of (i) an increase in the absolute amount of expression of each N-myc gene and (ii) an increase in the copy number of the N-myc gene. A second gene--which is amplified in many of the same lines as N-myc--is expressed to about the same degree in most human cell lines and primary tumors regardless of origin (when normalized to gene copy number). Thus, a change in the regulation of N-myc expression in neuroblastomas and certain other tumors results in greatly increased expression of each N-myc gene copy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kohl, N E -- Gee, C E -- Alt, F W -- 2-P01 CA 23767-06/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1984 Dec 14;226(4680):1335-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6505694" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; *Gene Amplification ; Gene Expression Regulation ; Humans ; Neuroblastoma/*genetics ; *Oncogenes ; RNA, Messenger/metabolism
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  • 7
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    Oncogene linked to growth factor receptor (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-02-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J L -- New York, N.Y. -- Science. 1984 Feb 24;223(4638):806.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6320370" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Cell Cycle ; Humans ; *Oncogenes ; Receptor, Epidermal Growth Factor ; *Receptors, Cell Surface
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  • 8
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    What do oncogenes do? (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-02-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J L -- New York, N.Y. -- Science. 1984 Feb 17;223(4637):673-4, 676.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6695176" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Genes, Viral ; Humans ; Neoplasms/*genetics ; *Oncogenes ; Repetitive Sequences, Nucleic Acid
    Print ISSN: 0036-8075
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  • 9
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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
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  • 10
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    Gene product of v-fgr onc: hybrid protein containing a portion of actin and a tyrosine-specific protein kinase (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-01-06
    Description: The nucleotide sequence of the region of Gardner-Rasheed feline sarcoma virus (GR-FeSV) encoding its primary translation product, p70gag-fgr, has been determined. From the nucleotide sequence, the amino acid sequence of this transforming protein was deduced. Computer analysis indicates that a portion of P70gag-fgr has extensive amino acid sequence homology with actin, a eukaryotic cytoskeletal protein. A second region of P70gag-fgr is closely related to the tyrosine-specific kinase gene family. Thus, the v-fgr oncogene appears to have arisen as a result of recombinational events involving two distinct cellular genes, one coding for a structural protein and the other for a protein kinase.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Naharro, G -- Robbins, K C -- Reddy, E P -- New York, N.Y. -- Science. 1984 Jan 6;223(4631):63-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6318314" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/analysis ; Amino Acid Sequence ; Base Sequence ; Computers ; Gene Products, gag ; *Genes, Viral ; *Oncogenes ; Protein Kinases/analysis ; Protein-Tyrosine Kinases ; Recombination, Genetic ; Retroviridae/*genetics ; Sarcoma Viruses, Feline/*genetics ; Viral Proteins/analysis/*genetics
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 11
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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
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  • 12
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    Antibodies to human c-myc oncogene product: evidence of an evolutionarily conserved protein induced during cell proliferation (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-08-17
    Description: Antisera to a synthetic c-myc peptide and to c-myc antigens synthesized from various portions of the human gene expressed in Escherichia coli were used in order to characterize the protein product of the human c-myc oncogene. Although the deduced molecular weight of the human c-myc protein is 49,000, these antisera precipitate a protein from human cells that migrates in sodium dodecyl sulfate-polyacrylamide gel as if its molecular weight were 65,000. In addition, the mouse c-myc protein, whether synthesized in cells or in a cell-free system directed by pure, synthetic messenger RNA, has analogous properties and is immunoprecipitated by the antiserum to the human c-myc protein. Similar proteins are immunoprecipitated from monkey, rat, hamster, and frog cells, suggesting evolutionary conservation of antigenic structure of the c-myc protein among vertebrates. In addition, and in a manner consistent with the behavior of its messenger RNA, the immunoprecipitable c-myc protein is sharply induced by the action of mitogens on resting human T cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Persson, H -- Hennighausen, L -- Taub, R -- DeGrado, W -- Leder, P -- New York, N.Y. -- Science. 1984 Aug 17;225(4663):687-93.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6431612" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antibodies, Neoplasm/*immunology ; Base Sequence ; *Cell Division ; Chickens ; Cricetinae ; DNA, Neoplasm/genetics ; DNA, Recombinant/metabolism ; Electrophoresis, Polyacrylamide Gel ; Haplorhini ; Humans ; Mice ; Mitogens/pharmacology ; Molecular Weight ; Neoplasm Proteins/genetics/*immunology ; *Oncogenes ; RNA, Messenger/genetics ; Rabbits ; Rats
    Print ISSN: 0036-8075
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  • 13
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    Amplification of N-myc in untreated human neuroblastomas correlates with advanced disease stage (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-06-08
    Description: A domain of DNA designated N-myc is amplified 20- to 140-fold in human neuroblastoma cell lines but not in cell lines from other tumor types. N-myc has now been found to be amplified in neuroblastoma tissue from 24 of 63 untreated patients (38 percent). The extent of amplification appears to be bimodal, with amplification of 100- to 300-fold in 12 cases and 3- to 10-fold in 10 others. Amplification was found in 0 of 15 patients with stage 1 or 2 disease, whereas 24 of 48 cases (50 percent) with stage 3 or 4 had evidence of N-myc amplification. These data indicate that N-myc amplification is a common event in untreated human neuroblastomas. Furthermore, N-myc amplification is highly correlated with advanced stages of disease (P less than 0.001) and with the ability to grow in vitro as an established cell line, both of which are associated with a poor prognosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brodeur, G M -- Seeger, R C -- Schwab, M -- Varmus, H E -- Bishop, J M -- CA02971/CA/NCI NIH HHS/ -- CA13539/CA/NCI NIH HHS/ -- CA17829/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1984 Jun 8;224(4653):1121-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6719137" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adult ; Aged ; Cell Line ; Child ; Child, Preschool ; DNA, Neoplasm/genetics ; Eye Neoplasms/genetics ; *Gene Amplification ; Humans ; Infant ; Lymphatic Metastasis ; Middle Aged ; Neuroblastoma/*genetics/physiopathology ; Nucleic Acid Hybridization ; *Oncogenes ; Prognosis ; Retinoblastoma/genetics
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  • 14
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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
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  • 15
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    Somatic activation of rasK gene in a human ovarian carcinoma (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-02-17
    Description: A tumor isolate from a patient with serous cystadenocarcinoma of the ovary contained an activated rasK gene detected hy transfection of NIH/3T3 cells. In contrast, DNA from normal cells of the same patient lacked transforming activity, indicating that activation of this transforming gene was the consequence of somatic mutation in the neoplastic cells. The transforming gene product displayed an electrophoretic mobility in sodium dodecyl sulfate-polyacrylamide gels that differed from the mobilities of rasK transforming proteins in other tumors, indicating that a previously undescribed mutation was responsible for activation of rasK in this ovarian carcinoma.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Feig, L A -- Bast, R C Jr -- Knapp, R C -- Cooper, G M -- CA07101/CA/NCI NIH HHS/ -- CA18689/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1984 Feb 17;223(4637):698-701.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6695178" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cell Line ; Cell Transformation, Neoplastic ; Cystadenocarcinoma/*genetics ; DNA, Neoplasm/genetics/isolation & purification ; Female ; Humans ; Lung Neoplasms/genetics ; Mice ; *Oncogenes ; Ovarian Neoplasms/*genetics ; Transfection
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 16
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    Isolation, characterization, and chromosome assignment of mouse N-ras gene from carcinogen-induced thymic lymphoma (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-09-07
    Description: Treatment of mice with the carcinogen N-methylnitrosourea results in the development of thymic lymphomas with frequent involvement of the N-ras oncogene. The activated mouse N-ras gene was isolated from one of these lymphomas and, by transformation in concert with restriction digestion, a map of the gene was prepared and its approximate boundaries were determined. By means of somatic cell hybrids the normal N-ras gene was found to be unlinked to other members of the ras gene family.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Guerrero, I -- Villasante, A -- D'Eustachio, P -- Pellicer, A -- CA-16239/CA/NCI NIH HHS/ -- GM-32105/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1984 Sep 7;225(4666):1041-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6089339" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cell Transformation, Neoplastic ; Chromosome Mapping ; Cloning, Molecular ; Cricetinae ; DNA Restriction Enzymes ; Deoxyribonuclease EcoRI ; Genetic Linkage ; Hybrid Cells ; Lymphoma/chemically induced/*genetics ; Methylnitrosourea ; Mice ; Mice, Inbred Strains ; *Oncogenes ; Thymus Neoplasms/chemically induced/*genetics
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  • 17
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    Activation of a c-K-ras oncogene by somatic mutation in mouse lymphomas induced by gamma radiation (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-09-14
    Description: Mouse tumors induced by gamma radiation are a useful model system for oncogenesis. DNA from such tumors contains an activated K-ras oncogene that can transform NIH 3T3 cells. This report describes the cloning of a fragment of the mouse K-ras oncogene containing the first exon from both a transformant in rat-2 cells and the brain of the same mouse that developed the tumor. Hybrid constructs containing one of the two pieces were made and only the plasmid including the first exon from the transformant gave rise to foci in NIH 3T3 cells. There was only a single base difference (G----A) in the exonic sequence, which changed glycine to aspartic acid in the transformant. By use of a synthetic oligonucleotide the presence of the mutation was demonstrated in the original tumor, ruling out modifications during DNA-mediated gene transfer and indicating that the alteration was present in the thymic lymphoma but absent from other nonmalignant tissue. The results are compatible with gamma radiation being a source of point mutations.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Guerrero, I -- Villasante, A -- Corces, V -- Pellicer, A -- CA-36327/CA/NCI NIH HHS/ -- GM-32036/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1984 Sep 14;225(4667):1159-62.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6474169" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cell Transformation, Neoplastic ; Cells, Cultured ; Cloning, Molecular ; Gamma Rays ; Lymphoma/*genetics ; Mice ; Mutation ; Neoplasms, Radiation-Induced/*genetics ; Nucleic Acid Hybridization ; *Oncogenes ; Rats
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  • 18
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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
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  • 19
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    Transforming potential of human c-sis nucleotide sequences encoding platelet-derived growth factor (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-08-10
    Description: The nucleotide sequence of a transforming human c-sis complementary DNA shows an open reading frame 723 base pairs in length located downstream from an in-phase terminator thymine-guanine-adenine codon. Sequences within this region were identical to those previously determined for the exons of the normal human c-sis gene. Thus, the predicted transforming product, a protein of 27,281 daltons, may be the actual precursor for normal human platelet-derived growth factor chain A.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Josephs, S F -- Ratner, L -- Clarke, M F -- Westin, E H -- Reitz, M S -- Wong-Staal, F -- New York, N.Y. -- Science. 1984 Aug 10;225(4662):636-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6740330" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cebidae ; Cell Transformation, Neoplastic/*metabolism ; Codon ; DNA, Neoplasm/genetics ; Humans ; Nucleic Acid Hybridization ; *Oncogenes ; Platelet-Derived Growth Factor/*genetics
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  • 20
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    A common onc gene sequence transduced by avian carcinoma virus MH2 and by murine sarcoma virus 3611 (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-02-24
    Description: A common cellular sequence was independently transduced by avian carcinoma virus MH2 (v-mht) and murine sarcoma virus (MSV) 3611 (v-raf). Comparison of the nucleotide sequences of v-mht and v-raf revealed a region of homology that extends over 969 nucleotides. The homology between the corresponding amino acids was about 95 percent with only 19 of 323 amino acids being different. With this example, 5 of the 19 known different viral onc genes have been observed in viruses of different taxonomic groups. These data indicate that (i) the number of cellular proto-onc genes is limited because, like other viruses of different taxonomic groups, MH2 and MSV 3611 have transduced the same onc gene-specific sequences from different cell species and (ii) that specific deletion and linkage of the same proto-onc sequences to different viral vector elements affect the oncogenic potential of the resulting viruses. The difference in transformation capabilities of MH2 and MSV 3611 serves as an example.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kan, N C -- Flordellis, C S -- Mark, G E -- Duesberg, P H -- Papas, T S -- CA11426/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1984 Feb 24;223(4638):813-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6320371" target="_blank"〉PubMed〈/a〉
    Keywords: Alpharetrovirus/*genetics ; Animals ; Base Sequence ; Chickens/genetics ; Genes, Viral ; Mice ; *Oncogenes ; Sarcoma Viruses, Murine/*genetics ; Species Specificity ; Transduction, Genetic
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  • 21
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    Primary structure of v-raf: relatedness to the src family of oncogenes (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-04-20
    Description: A replication-defective, acute transforming retrovirus (murine sarcoma virus 3611) was isolated from mouse and molecularly cloned. The nucleotide sequence of 1.5 kilobases encompassing the transforming gene (v-raf) was determined. This sequence, which predicts the amino acid sequence of a gag-raf fusion protein, terminates 180 nucleotides from the 3' end of the acquired cellular sequence. Comparison of the predicted amino acid sequence of v-raf with the predicted amino acid sequences of other oncogenes reveals significant homologies to the src family of oncogenes. There is a lack of homology within the sequence of the tyrosine acceptor domain described for the phosphotyrosine kinase members of the src family of transforming proteins. Phylogenetic arrangement of this family of oncogenes suggests that tyrosine-specific phosphorylation may be a recently acquired activity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mark, G E -- Rapp, U R -- New York, N.Y. -- Science. 1984 Apr 20;224(4646):285-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6324342" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Binding Sites ; Biological Evolution ; Cell Transformation, Neoplastic ; Cell Transformation, Viral ; DNA Restriction Enzymes ; Gene Products, gag ; *Genes, Viral ; Mice ; *Oncogenes ; Protein Biosynthesis ; Protein Kinases/metabolism ; Protein-Tyrosine Kinases ; Sarcoma Viruses, Murine/*genetics ; Transcription, Genetic ; Tyrosine/metabolism ; Viral Proteins/analysis/*genetics
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  • 22
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    Oncogene linked to cell regulatory system (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-11-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J L -- New York, N.Y. -- Science. 1984 Nov 2;226(4674):527-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6093250" target="_blank"〉PubMed〈/a〉
    Keywords: Adenylyl Cyclases/*physiology ; Animals ; Cell Transformation, Neoplastic/metabolism ; Cyclic AMP/physiology ; Drosophila ; Guanosine Triphosphate/physiology ; Humans ; *Oncogenes ; Rodentia ; Yeasts
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  • 23
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    Tumor-prone mice--and myc (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-11-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J L -- New York, N.Y. -- Science. 1984 Nov 16;226(4676):823.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6494912" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Female ; Mice ; Mice, Mutant Strains/*genetics ; Neoplasms, Experimental/*genetics ; *Oncogenes ; Pregnancy
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  • 24
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    The N-myc oncogene in neural tumors (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-06-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J L -- New York, N.Y. -- Science. 1984 Jun 8;224(4653):1088.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6719134" target="_blank"〉PubMed〈/a〉
    Keywords: Child ; Child, Preschool ; Eye Neoplasms/*genetics ; Humans ; Infant ; Neuroblastoma/*genetics ; *Oncogenes ; Retinoblastoma/*genetics
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  • 25
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    New oncogene targets? (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-04-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J L -- New York, N.Y. -- Science. 1984 Apr 20;224(4646):272.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6324341" target="_blank"〉PubMed〈/a〉
    Keywords: 1-Phosphatidylinositol 4-Kinase ; Avian Sarcoma Viruses/*genetics ; *Cell Transformation, Neoplastic ; Diglycerides/metabolism ; Genes, Viral ; Inositol 1,4,5-Trisphosphate ; Inositol Phosphates/metabolism ; *Oncogenes ; Phosphatidylinositol Phosphates ; Phosphatidylinositols/*metabolism ; Phosphorylation ; Phosphotransferases/*genetics/metabolism
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  • 26
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    Oncogenes amplified in cancer cells (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-01-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J L -- New York, N.Y. -- Science. 1984 Jan 6;223(4631):40-1.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6691135" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cell Transformation, Neoplastic ; Chromosome Aberrations ; *Gene Amplification ; Humans ; Leukemia/genetics ; Lung Neoplasms/genetics ; Neoplasms/*genetics/metabolism ; Neuroblastoma/genetics ; *Oncogenes ; RNA, Messenger/biosynthesis ; RNA, Neoplasm/biosynthesis ; Translocation, Genetic
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  • 27
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    Perusing the myc gene (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-02-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J L -- New York, N.Y. -- Science. 1984 Feb 17;223(4637):675.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6695177" target="_blank"〉PubMed〈/a〉
    Keywords: Burkitt Lymphoma/*genetics ; Chromosome Aberrations ; Chromosome Disorders ; Chromosomes, Human, 16-18 ; Chromosomes, Human, 6-12 and X ; Humans ; *Oncogenes
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  • 28
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    Mapping of the human Blym-1 transforming gene activated in Burkitt lymphomas to chromosome 1 (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-01-13
    Description: Blym-1, a transforming gene detected by transfection of NIH 3T3 cells with DNA from Burkitt lymphomas, was mapped to the short arm of chromosome 1 (1p32) by chromosomal in situ hybridization. The Blym-1 gene was not physically linked to the cellular myc oncogene or to any of the immunoglobulin gene loci implicated in the characteristic chromosomal translocations in Burkitt lymphoma.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Morton, C C -- Taub, R -- Diamond, A -- Lane, M A -- Cooper, G M -- Leder, P -- CA-21082/CA/NCI NIH HHS/ -- CA-33108/CA/NCI NIH HHS/ -- GM-17088/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1984 Jan 13;223(4632):173-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6691143" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; Burkitt Lymphoma/*genetics ; Chromosome Aberrations ; Chromosome Mapping ; *Chromosomes, Human, 1-3 ; Genetic Linkage ; Humans ; Immunoglobulins/genetics ; Male ; Nucleic Acid Hybridization ; *Oncogenes ; Translocation, Genetic
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  • 29
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    Retinoblastoma: clues to human oncogenesis (1984)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1984-03-09
    Description: The retinoblastoma gene can be considered a model for a class of recessive human cancer genes that have a "suppressor" or "regulatory" function. The loss or inactivation of both alleles of this gene appears to be a primary mechanism in the development of retinoblastoma. Such a mechanism is in direct contrast to that of putative human oncogenes which are thought to induce tumorigenesis following activation or alteration. The high incidence of second primary tumors among patients who inherit one inactive retinoblastoma allele also suggests that this cancer gene plays a key role in the etiology of several other primary malignancies. Finally, the observation that extra nonrandom copies of specific chromosomal regions occur in some of these tumors provides circumstantial evidence that an "expressor" gene (possibly an oncogene) may be involved in retinoblastoma development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Murphree, A L -- Benedict, W F -- EY-02715/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 1984 Mar 9;223(4640):1028-33.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6320372" target="_blank"〉PubMed〈/a〉
    Keywords: Adenocarcinoma/genetics ; Alleles ; Child ; Chromosome Deletion ; Chromosome Mapping ; Chromosomes, Human, 13-15 ; Chromosomes, Human, 6-12 and X ; Eye Neoplasms/*genetics ; Genes, Recessive ; Genotype ; Humans ; Kidney Neoplasms/genetics ; Mutation ; Neuroblastoma/genetics ; *Oncogenes ; Polymorphism, Genetic ; Retinoblastoma/*genetics ; *Suppression, Genetic ; Translocation, Genetic ; Wilms Tumor/genetics
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  • 30
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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
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  • 31
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    Nuclear localization and DNA binding properties of a protein expressed by human c-myc oncogene (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-08-17
    Description: Antisera to the human cellular myc oncogene product were used to identify a human c-myc specific protein with a molecular weight of 65,000. Subcellular fractionation showed that the human c-myc protein is predominantly found in the cell nucleus. The p65Kc-myc protein binds to double- and single-stranded DNA as measured by a DNA affinity chromatography assay.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Persson, H -- Leder, P -- New York, N.Y. -- Science. 1984 Aug 17;225(4663):718-21.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6463648" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; Cell Nucleus/*metabolism ; Cell Transformation, Neoplastic/metabolism ; Chromatography, Affinity ; DNA, Neoplasm/*metabolism ; Humans ; Neoplasm Proteins/*metabolism ; *Oncogenes ; RNA, Messenger/metabolism ; Subcellular Fractions/metabolism
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  • 32
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    Activation of the c-myb locus by viral insertional mutagenesis in plasmacytoid lymphosarcomas (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-11-30
    Description: Rearrangement in the c-myb locus of each of four independently derived BALB/c plasmacytoid lymphosarcoma (ABPL's) is due to the insertion of a defective Moloney murine leukemia virus (M-MuLV) into a 1.5-kilobase-pair stretch of cellular DNA at the 5' end of the v-myb-related sequences. This retroviral insertion is associated with abnormal transcription of myb sequences and probably represents a step in the neoplastic transformation of ABPL cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shen-Ong, G L -- Potter, M -- Mushinski, J F -- Lavu, S -- Reddy, E P -- New York, N.Y. -- Science. 1984 Nov 30;226(4678):1077-80.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6093260" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Chromosome Deletion ; Cloning, Molecular ; DNA Restriction Enzymes ; DNA Transposable Elements ; *Genes, Viral ; Lymphoma, Non-Hodgkin/genetics/*microbiology ; Mice ; Mice, Inbred BALB C ; Moloney murine leukemia virus/*genetics ; *Mutation ; 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
    Published by American Association for the Advancement of Science (AAAS)
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  • 33
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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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  • 34
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    Transcription and promoter usage of the myc gene in normal somatic and spermatogenic cells (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-11-09
    Description: In somatic cells the level of myc transcription is not restricted to particular cell types but correlates closely with the rate of cell division. Such transcription involves the use of two active myc promoters and produces two messenger RNA species that are differentially represented among the transcripts of different tissues. In apparent contrast to somatic cells, mitotically and meiotically dividing germ cells have very few myc transcripts and appear to proliferate, at least for a few divisions, in the absence of myc transcription. These results raise interesting questions regarding the role of the myc gene product in terminally differentiating cells, particularly of the germ line series.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stewart, T A -- Bellve, A R -- Leder, P -- HD06645/HD/NICHD NIH HHS/ -- HD08270/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1984 Nov 9;226(4675):707-10.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6494906" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; Cell Division ; Male ; Meiosis ; Mice ; *Oncogenes ; *Operon ; RNA, Messenger/metabolism ; Sertoli Cells/physiology ; Spermatocytes/physiology ; *Spermatogenesis ; *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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  • 35
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    A transforming ras gene in tumorigenic guinea pig cell lines initiated by diverse chemical carcinogens (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-03-16
    Description: Fetal guinea pig cells were transformed by treatment with four different chemical carcinogens including nitroso compounds and polycyclic hydrocarbons. As a consequence of this treatment, oncogenes capable of transforming NIH/3T3 cells became activated in each of five independently established clonal guinea pig cell lines. Molecular characterization of representative NIH/3T3 transformants revealed that the same oncogene was present in each of the cell lines tested. Moreover, detection of this transforming gene paralleled the acquisition of tumorigenic properties by these neoplastic cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sukumar, S -- Pulciani, S -- Doniger, J -- DiPaolo, J A -- Evans, C H -- Zbar, B -- Barbacid, M -- New York, N.Y. -- Science. 1984 Mar 16;223(4641):1197-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6322298" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Benzo(a)pyrene ; Benzopyrenes ; *Carcinogens ; Cell Division ; Cell Line ; *Cell Transformation, Neoplastic ; DNA Restriction Enzymes ; Diethylnitrosamine ; *Gene Expression Regulation ; Genes, Viral ; Guinea Pigs ; Methylcholanthrene ; Methylnitronitrosoguanidine ; Mice ; *Oncogenes ; Retroviridae/genetics
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 36
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    An activated rasN gene: detected in late but not early passage human PA1 teratocarcinoma cells (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-08-10
    Description: Early passages of the human teratocarcinoma cell line PA1 are not tumorigenic in nude mice, while late passages are. A transforming gene present in late passages of PA1 cells was isolated as a biologically active molecular clone and is a new isolate of the human rasN locus. Its transforming activity is due to a single G---A (G, guanine; A, adenine) point mutation at the codon for amino acid 12 which changes the codon for glycine so that an aspartic acid residue is expressed. In contrast to late passage PA1 cells (passages 106, 330, and 338), DNA from the PA1 cell line at early passages (passage 36) does not yield rasN foci in DNA transfection assays. Thus, the presence of an activated rasN in PA1 cells correlates with enhanced tumorigenicity of the cell line and, more importantly, may have arisen during cell culture in vitro.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tainsky, M A -- Cooper, C S -- Giovanella, B C -- Vande Woude, G F -- New York, N.Y. -- Science. 1984 Aug 10;225(4662):643-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6740333" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cell Line ; Cell Transformation, Neoplastic/metabolism ; DNA, Neoplasm/genetics ; Humans ; Mice ; Mice, Nude ; *Oncogenes ; Teratoma/*genetics ; Time Factors
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 37
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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
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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