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  • 1
    Publication Date: 1989-10-27
    Description: Allele loss is a hallmark of chromosome regions harboring recessive oncogenes. Lung cancer frequently demonstrates loss of heterozygosity on 17p. Recent evidence suggests that the p53 gene located on 17p13 has many features of such an antioncogene. The p53 gene was frequently mutated or inactivated in all types of human lung cancer. The genetic abnormalities of p53 include gross changes such as homozygous deletions and abnormally sized messenger RNAs along with a variety of point or small mutations, which map to the p53 open reading frame and change amino acid sequence in a region highly conserved between mouse and man. In addition, very low or absent expression of p53 messenger RNA in lung cancer cell lines compared to normal lung was seen. These findings, coupled with the previous demonstration of 17p allele loss in lung cancer, strongly implicate p53 as an anti-oncogene whose disruption is involved in the pathogenesis of human lung cancer.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Takahashi, T -- Nau, M M -- Chiba, I -- Birrer, M J -- Rosenberg, R K -- Vinocour, M -- Levitt, M -- Pass, H -- Gazdar, A F -- Minna, J D -- New York, N.Y. -- Science. 1989 Oct 27;246(4929):491-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Cancer Institute-Navy Medical Oncology Branch, Bethesda, MD 20814.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2554494" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; Carcinoid Tumor/genetics ; Carcinoma, Non-Small-Cell Lung/genetics ; Carcinoma, Small Cell/genetics ; Chromosomes, Human, Pair 17 ; DNA, Neoplasm/genetics ; Gene Amplification ; Humans ; Lung Neoplasms/*genetics ; Mutation ; Oncogene Proteins/*genetics ; Phosphoproteins/*genetics ; RNA, Messenger/genetics ; RNA, Neoplasm/genetics ; Ribonucleases ; Tumor Cells, Cultured ; Tumor Suppressor Protein p53
    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
    Publication Date: 1989-01-01
    Description: The hematopoietic growth factor interleukin-3 (IL-3) promotes the proliferation and maturation of pluripotent myeloid progenitor cells. In the immune system, IL-3 is synthesized by mitogen or antigen- stimulated T lymphocytes. We demonstrate the expression of IL-3 mRNA in mouse brain by in situ hybridization histochemistry and Northern blot analysis. The IL-3 mRNA is localized in discrete areas of the brain and can be found in neuronal cell body and astrocytes. Northern analysis of cerebellar RNA, compared with mRNA extracted from WEHI-3 cells, showed a single hybridization band, approximately 1.2 kb, suggesting similar processing between brain and myeloid cells. The molecular evidence and previous observations of IL-3-like biologic activity found in the brain suggest a potential role for IL-3 in the neurobiology of the CNS.
    Print ISSN: 0006-4971
    Electronic ISSN: 1528-0020
    Topics: Biology , Medicine
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  • 3
    Publication Date: 1989-01-01
    Description: The hematopoietic growth factor interleukin-3 (IL-3) promotes the proliferation and maturation of pluripotent myeloid progenitor cells. In the immune system, IL-3 is synthesized by mitogen or antigen- stimulated T lymphocytes. We demonstrate the expression of IL-3 mRNA in mouse brain by in situ hybridization histochemistry and Northern blot analysis. The IL-3 mRNA is localized in discrete areas of the brain and can be found in neuronal cell body and astrocytes. Northern analysis of cerebellar RNA, compared with mRNA extracted from WEHI-3 cells, showed a single hybridization band, approximately 1.2 kb, suggesting similar processing between brain and myeloid cells. The molecular evidence and previous observations of IL-3-like biologic activity found in the brain suggest a potential role for IL-3 in the neurobiology of the CNS.
    Print ISSN: 0006-4971
    Electronic ISSN: 1528-0020
    Topics: Biology , Medicine
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