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  • 1
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    The Met proto-oncogene mesenchymal to epithelial cell conversion (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-01-07
    Description: Coexpression of the human Met receptor and its ligand, hepatocyte growth factor/scatter factor (HGF/SF), in NIH 3T3 fibroblasts causes the cells to become tumorigenic in nude mice. The resultant tumors display lumen-like morphology, contain carcinoma-like focal areas with intercellular junctions resembling desmosomes, and coexpress epithelial (cytokeratin) and mesenchymal (vimentin) cytoskeletal markers. The tumor cells also display enhanced expression of desmosomal and tight-junction proteins. The apparent mesenchymal to epithelial conversion of the tumor cells mimics the conversion that occurs during embryonic kidney development, suggesting that Met-HGF/SF signaling plays a role in this process as well as in tumors that express both epithelial and mesenchymal markers.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tsarfaty, I -- Rong, S -- Resau, J H -- Rulong, S -- da Silva, P P -- Vande Woude, G F -- N01-CO-74101/CO/NCI NIH HHS/ -- New York, N.Y. -- Science. 1994 Jan 7;263(5143):98-101.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉ABL-Basic Research Program, National Cancer Institute (NCI)-Frederick Cancer Research and Development Center, MD 21702-1201.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7505952" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Animals ; *Cell Transformation, Neoplastic ; Desmosomes/ultrastructure ; Epithelial Cells ; Hepatocyte Growth Factor/metabolism/pharmacology ; Keratins/biosynthesis ; Kidney/embryology/metabolism ; Mesoderm/cytology ; Mice ; Mice, Nude ; Neoplasms, Experimental/metabolism/*pathology ; Proto-Oncogene Proteins/genetics/*metabolism ; Proto-Oncogene Proteins c-met ; *Proto-Oncogenes ; Receptor Protein-Tyrosine Kinases/genetics/*metabolism ; Signal Transduction ; Transfection ; Vimentin/biosynthesis
    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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    Abnormal centrosome amplification in the absence of p53 (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-03-22
    Description: The centrosome plays a vital role in mitotic fidelity, ensuring establishment of bipolar spindles and balanced chromosome segregation. Centrosome duplication occurs only once during the cell cycle and is therefore highly regulated. Here, it is shown that in mouse embryonic fibroblasts (MEFs) lacking the p53 tumor suppressor protein, multiple copies of functionally competent centrosomes are generated during a single cell cycle. In contrast, MEFs prepared from normal mice or mice deficient in the retinoblastoma tumor suppressor gene product do not display these abnormalities. The abnormally amplified centrosomes profoundly affect mitotic fidelity, resulting in unequal segregation of chromosomes. These observations implicate p53 in the regulation of centrosome duplication and suggest one possible mechanism by which the loss of p53 may cause genetic instability.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fukasawa, K -- Choi, T -- Kuriyama, R -- Rulong, S -- Vande Woude, G F -- New York, N.Y. -- Science. 1996 Mar 22;271(5256):1744-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉ABL-Basic Research Program, National Cancer Institute, Frederick Cancer Research and Development Center, Frederick, MD 21702-1201, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8596939" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood ; Cells, Cultured ; Centrosome/*metabolism ; Culture Media ; Fibroblasts ; Genes, Retinoblastoma ; Genes, p53 ; *Interphase ; Mice ; *Mitosis ; Spindle Apparatus/metabolism/ultrastructure ; Tumor Suppressor Protein p53/*physiology
    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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  • 3
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    The met proto-oncogene receptor and lumen formation (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-08-28
    Description: The met proto-oncogene product (Met) and its ligand, hepatocyte growth factor/scatter factor (HGF/SF), have been implicated in cell mitogenic response, cell motility, and the promotion of the ordered spatial arrangement of tissue. By means of confocal laser-scanning microscopy, it was shown that Met is expressed in cells bordering lumen-like structures that resemble ducts in the human mammary cell line T47D. In human breast tissue biopsies, Met staining was intense in normal cells bordering mammary ducts but was reduced in adjacent tumor tissue. Met staining in lumen-forming organs colocalizes with staining of antibody to phosphotyrosine, which suggests that the Met receptor and its substrates may be activated in lumen structures or ducts. HGF/SF treatment of human epithelial carcinoma cell lines resulted in the formation of lumen-like structures in vitro. Reduced expression of Met could be related to the extent of tumor cell differentiation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tsarfaty, I -- Resau, J H -- Rulong, S -- Keydar, I -- Faletto, D L -- Vande Woude, G F -- N01-C0-74101/PHS HHS/ -- New York, N.Y. -- Science. 1992 Aug 28;257(5074):1258-61.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉ABL-Basic Research Program, National Cancer Institute-Frederick Cancer Research and Development Center, Frederick, MD 21702.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1387731" target="_blank"〉PubMed〈/a〉
    Keywords: Adenocarcinoma/metabolism/pathology ; Animals ; Breast Neoplasms/metabolism/pathology ; Cell Differentiation/genetics ; Chromosomes, Human, Pair 7 ; Colonic Neoplasms/chemically induced/metabolism/pathology ; Digestive System/metabolism ; Dose-Response Relationship, Drug ; Growth Substances/pharmacology/*physiology ; Hepatocyte Growth Factor ; Humans ; Mice ; Mice, Inbred BALB C ; Microscopy, Fluorescence ; Microscopy, Immunoelectron ; Proto-Oncogene Proteins/*physiology ; Proto-Oncogene Proteins c-met
    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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  • 4
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    Mos/mitogen-activated protein kinase can induce early meiotic phenotypes in the absence of maturation-promoting factor: a novel system for analyzing spindle formation during meiosis I. (1996)
    National Academy of Sciences
    Details
    Publication Date: 1996-05-14
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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