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  • 1
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    Bone marrow origin of hepatic macrophages (Kupffer cells) in humans (1978)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1978-09-08
    Description: Hepatic macrophages (Kupffer cells) from two male recipients of bone marrow transplants from females were studied for fluorescent Y body staining and sex chromatin (Barr body). After the transplant, macrophages had the sex karyotype of the donor, indicating that human hepatic macrophages originate in bone marrow.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gale, R P -- Sparkes, R S -- Golde, D W -- New York, N.Y. -- Science. 1978 Sep 8;201(4359):937-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/356266" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; *Bone Marrow Cells ; Bone Marrow Transplantation ; Cell Differentiation ; Cell Movement ; Female ; Graft vs Host Disease/immunology ; Humans ; Kupffer Cells/*cytology ; Male ; Transplantation, Homologous
    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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    Purified human granulocyte-macrophage colony-stimulating factor: direct action on neutrophils (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-12-14
    Description: Neutrophil migration inhibition factor from T lymphocytes (NIF-T) is a lymphokine that acts to localize granulocytes. Medium conditioned by the Mo human T-lymphoblast cell line was used to purify NIF-T, a glycoprotein with a molecular weight of 22,000. The NIF-T was found to potently stimulate the growth of granulocyte and macrophage colonies from human bone marrow and colony formation by the KG-1 myeloid leukemia cell line. Thus a human lymphokine (NIF-T) that modulates the activities of mature neutrophilic granulocytes is also a colony-stimulating factor acting on precursors to induce growth and differentiation of new effector cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gasson, J C -- Weisbart, R H -- Kaufman, S E -- Clark, S C -- Hewick, R M -- Wong, G G -- Golde, D W -- CA 30280/CA/NCI NIH HHS/ -- CA 30388/CA/NCI NIH HHS/ -- CA 32737/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1984 Dec 14;226(4680):1339-42.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6390681" target="_blank"〉PubMed〈/a〉
    Keywords: Bone Marrow Cells ; Cell Division ; Cell Line ; Chromatography, High Pressure Liquid ; Colony-Stimulating Factors/*isolation & purification ; Electrophoresis, Polyacrylamide Gel ; Granulocytes/*cytology ; Humans ; Leukocyte Migration-Inhibitory Factors/*pharmacology ; Lymphokines/*pharmacology ; Macrophages/*cytology ; Molecular Weight
    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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    Proliferation of astroglia and oligodendroglia in response to human T cell-derived factors (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-06-29
    Description: Human T lymphocytes transformed by human T cell leukemia-lymphoma viruses or activated by lectins were found to produce stimulating factors that promoted both proliferation and maturation of oligodendroglial and astroglial cells in vitro.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Merrill, J E -- Kutsunai, S -- Mohlstrom, C -- Hofman, F -- Groopman, J -- Golde, D W -- CA 30388/CA/NCI NIH HHS/ -- CA 32737/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1984 Jun 29;224(4656):1428-30.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6610212" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Animals ; Astrocytes/*drug effects ; Cell Division/*drug effects ; Cell Line ; Growth Substances/*pharmacology ; Humans ; Lymphocyte Activation ; Lymphokines/pharmacology ; Neuroglia/*drug effects ; Oligodendroglia/*drug effects ; Rats ; Receptors, Fc/metabolism ; T-Lymphocytes/*physiology
    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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    Identification of the putative transforming protein of the human T-cell leukemia viruses HTLV-I and HTLV-II (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-10-05
    Description: The human T-cell leukemia viruses HTLV-I and HTLV-II are unique among the transforming retroviruses of vertebrates in their ability to transform human T cells in vitro and in their close association with human malignancies (T-cell lymphomas and leukemia). Their genomes are relatively simple, containing the genes gag, pol, env, and a 3' region termed "X." This 3' region may be responsible for the transforming potential of the viruses. The existence of proteins encoded by the 3' region has been postulated on the basis of multiple open reading frames. In the present study this region is shown to contain a gene encoding a protein of 40 kilodaltons in HTLV-I and 37 kilodaltons in HTLV-II. It is proposed that these proteins be called, respectively, p40xI and p37xII.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Slamon, D J -- Shimotohno, K -- Cline, M J -- Golde, D W -- Chen, I S -- CA 16042/CA/NCI NIH HHS/ -- CA 32737/CA/NCI NIH HHS/ -- RR 00865/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 1984 Oct 5;226(4670):61-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6089351" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; B-Lymphocytes/microbiology ; Cell Line ; *Cell Transformation, Viral ; Deltaretrovirus/analysis/*genetics/physiology ; *Genes, Viral ; Humans ; Immune Sera ; Molecular Weight ; T-Lymphocytes/*microbiology ; Trans-Activators ; Viral Proteins/genetics/immunology/*physiology
    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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    Acute myelogenous leukemia: a human cell line responsive to colony-stimulating activity (1978)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1978-06-09
    Description: A permanent human cell line that maintains the granulocytic characteristics of acute myelogenous leukemia cells has been established. The cells of this line form myeloid colonies in soft gel culture in the presence of human colony-stimulating activity. The cell line may be useful for studying human acute myelogenous leukemia and the mechanism of response to colony-stimulating activity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Koeffler, H P -- Golde, D W -- New York, N.Y. -- Science. 1978 Jun 9;200(4346):1153-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/306682" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Division/drug effects ; *Cell Line ; Chromosome Aberrations/genetics ; Chromosome Disorders ; Colony-Stimulating Factors/*pharmacology ; Glycoproteins/*pharmacology ; Granulocytes/pathology ; Humans ; Leukemia, Myeloid, Acute/genetics/*pathology ; Male ; Middle Aged ; Receptors, Antigen, B-Cell/analysis
    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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    Studies of the putative transforming protein of the type I human T-cell leukemia virus (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-06-21
    Description: The putative transforming protein of the type I human T-cell leukemia virus (HTLV-1) is a 40-kilodalton protein encoded by the X region and is termed p40XI. On the basis of both subcellular fractionation techniques and immunocytochemical analysis, it is now shown that p40XI is a nuclear protein with a relatively short half-life (120 minutes). It is synthesized de novo in considerable quantities in a human T-cell line infected with and transformed by the virus in vitro, and it is not packaged in detectable amounts in the extracellular virus.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Slamon, D J -- Press, M F -- Souza, L M -- Murdock, D C -- Cline, M J -- Golde, D W -- Gasson, J C -- Chen, I S -- CA 32737/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1985 Jun 21;228(4706):1427-30.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2990027" target="_blank"〉PubMed〈/a〉
    Keywords: Antigens, Polyomavirus Transforming ; Antigens, Viral, Tumor/immunology/*metabolism ; Cell Fractionation ; Cell Line ; Cell Nucleus/metabolism ; Cell Transformation, Viral ; Deltaretrovirus/*metabolism ; Half-Life ; Humans ; Immune Sera ; Precipitin Tests ; Viral Proteins/immunology/*metabolism
    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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    HTLV x-gene product: requirement for the env methionine initiation codon (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-06-28
    Description: The human T-cell leukemia viruses (HTLV) are replication-competent retroviruses whose genomes contain gag, pol, and env genes as well as a fourth gene, termed x, which is believed to be the transforming gene of HTLV. The product of the x gene is now shown to be encoded by a 2.1-kilobase messenger RNA derived by splicing of at least two introns. By means of S1 nuclease mapping of this RNA and nucleic acid sequence analysis of a complementary DNA clone, the complete primary structure of the x-gene product has been determined. It is encoded by sequences containing the env initiation codon and one nucleotide of the next codon spliced to the major open reading frame of the HTLV-I and HTLV-II x gene.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wachsman, W -- Golde, D W -- Temple, P A -- Orr, E C -- Clark, S C -- Chen, I S -- CA 30388/CA/NCI NIH HHS/ -- CA 32737/CA/NCI NIH HHS/ -- CA 38597/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1985 Jun 28;228(4707):1534-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2990032" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cell Transformation, Viral ; Codon ; Deltaretrovirus/*genetics ; Electrophoresis, Polyacrylamide Gel ; Humans ; Methionine/*genetics ; Rats ; Viral Proteins/*analysis
    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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    Evidence for the involvement of GM-CSF and FMS in the deletion (5q) in myeloid disorders (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-02-28
    Description: By in situ chromosomal hybridization, the GM-CSF and FMS genes were localized to human chromosome 5 at bands q23 to q31, and at band 5q33, respectively. These genes encode proteins involved in the regulation of hematopoiesis, and are located within a chromosome region frequently deleted in patients with neoplastic myeloid disorders. Both genes were deleted in the 5q-chromosome from bone marrow cells of two patients with refractory anemia and a del(5)(q15q33.3). The GM-CSF gene alone was deleted in a third patient with acute nonlymphocytic leukemia (ANLL) who has a smaller deletion, del(5)(q22q33.1). Leukemia cells from a fourth patient who has ANLL and does not have a del(5q), but who has a rearranged chromosome 5 that is missing bands q31.3 to q33.1 [ins(21;5)(q22;q31.3q33.1)] were used to sublocalize these genes; both genes were present on the rearranged chromosome 5. Thus, the deletion of one or both of these genes may be important in the pathogenesis of myelodysplastic syndromes or of ANLL.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Le Beau, M M -- Westbrook, C A -- Diaz, M O -- Larson, R A -- Rowley, J D -- Gasson, J C -- Golde, D W -- Sherr, C J -- CA 16910/CA/NCI NIH HHS/ -- CA 23954/CA/NCI NIH HHS/ -- CA 30388/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1986 Feb 28;231(4741):984-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3484837" target="_blank"〉PubMed〈/a〉
    Keywords: Anemia, Refractory/genetics ; Bone Marrow Diseases/*genetics ; *Chromosome Deletion ; Chromosome Mapping ; *Chromosomes, Human, 4-5 ; Colony-Stimulating Factors/*genetics ; Humans ; Leukemia/genetics ; *Proto-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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  • 9
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    Cytokines alter production of HIV-1 from primary mononuclear phagocytes (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-09-23
    Description: Some strains of human immunodeficiency virus type 1 (HIV-1) can infect primary monocytes and monocyte-derived macrophages in vitro. In this report, the effect of cytokines on the production of one of these strains that shows a tropism for mononuclear phagocytes, designated HIV-1JR-FL, was studied. Primary peripheral blood mononuclear phagocytes infected with HIV-1JR-FL were treated with the hematopoietic factors: granulocyte colony-stimulating factor (G-CSF), granulocyte-macrophage colony-stimulating factor (GM-CSF), interleukin-3 (IL-3), macrophage colony-stimulating factor (M-CSF), and gamma-interferon (gamma-IFN). The M-CSF, GM-CSF, IL-3, and gamma-IFN were able to alter HIV-1 production under different conditions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Koyanagi, Y -- O'Brien, W A -- Zhao, J Q -- Golde, D W -- Gasson, J C -- Chen, I S -- New York, N.Y. -- Science. 1988 Sep 23;241(4873):1673-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunology, UCLA School of Medicine 90024.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3047875" target="_blank"〉PubMed〈/a〉
    Keywords: Biological Products/*pharmacology ; Colony-Stimulating Factors/pharmacology ; Cytokines ; Granulocyte-Macrophage Colony-Stimulating Factor ; Growth Substances/pharmacology ; HIV/*physiology ; Humans ; Interleukin-3/pharmacology ; Kinetics ; Macrophages ; Monocytes/*microbiology ; *Virus Replication
    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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  • 10
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    Expression of the 3' terminal region of human T-cell leukemia viruses (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-10-12
    Description: Human T-cell leukemia viruses (HTLV) are closely associated with some human T-cell leukemias and lymphomas. A unique 3' region of the HTLV genome is believed to be involved in HTLV-induced cellular transformation, although the function of this region has yet to be determined. A subgenomic messenger RNA transcribed from this region of HTLV has now been characterized. These results provide direct evidence for the expression of a novel gene in HTLV.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wachsman, W -- Shimotohno, K -- Clark, S C -- Golde, D W -- Chen, I S -- CA 09297/CA/NCI NIH HHS/ -- CA 30388/CA/NCI NIH HHS/ -- CA 32737/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1984 Oct 12;226(4671):177-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6091270" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; Cell Line ; Cell Transformation, Viral ; Deltaretrovirus/*genetics/physiology ; *Genes, Viral ; Humans ; Nucleic Acid Hybridization ; RNA Splicing ; RNA, Messenger/genetics ; RNA, Viral/*genetics ; T-Lymphocytes ; Transcription, Genetic ; Viral Proteins/*genetics
    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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