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Novel mutations of the MET proto-oncogene in papillary renal carcinomas

  1. Author:
    Schmidt, L.
    Junker, K.
    Nakaigawa, N.
    Kinjerski, T.
    Weirich, G.
    Miller, M.
    Lubensky, I.
    Neumann, H. P. H.
    Brauch, H.
    Decker, J.
    Vocke, C.
    Brown, J. A.
    Jenkins, R.
    Richard, S.
    Bergerheim, U.
    Gerrard, B.
    Dean, M.
    Linehan, W. M.
    Zbar, B.

  2. Author Address

    Schmidt L NCI, Frederick Canc Res & Dev Ctr, Immunobiol Lab Bldg 560 Rm 12-29 Frederick, MD 21702 USA NCI, Frederick Canc Res & Dev Ctr, Immunobiol Lab Frederick, MD 21702 USA NCI, Frederick Canc Res & Dev Ctr, SAIC Frederick, Intramural Res Support Program Frederick, MD 21702 USA NCI, Frederick Canc Res & Dev Ctr, ABL Basic Res Program, Macromol Struct Lab Frederick, MD 21702 USA NCI, Frederick Canc Res & Dev Ctr, Lab Genom Divers Frederick, MD 21702 USA NIH, Urol Oncol Branch Bethesda, MD 20892 USA NIH, Pathol Lab Bethesda, MD 20892 USA Univ Freiburg D-79106 Freiburg Germany Univ Hamburg, Womens Clin, Hamburg Eppendorf UKE D-20246 Hamburg Germany Univ Mainz D-55131 Mainz Germany Mayo Clin & Mayo Fdn, Div Lab Genet Rochester, MN 55905 USA Karolinska Inst Stockholm Sweden Hop Bicetre, Dept Urol Paris France EPHE, Lab Neuoroncol F-75006 Paris France Univ Jena, Dept Urol D-07743 Jena Germany David Grant Med Ctr Travis AFB, CA 94535 USA
    1. Year: 1999
  2. Journal: Oncogene
    1. 18
    2. 14
    3. Pages: 2343-2350
  4. Type of Article: Article
  1. Abstract:

    Hereditary papillary renal carcinoma (HPRC) is characterized by multiple, bilateral papillary renal carcinomas. Previously, we demonstrated missense mutations in the tyrosine kinase domain of the MET proto-oncogene in HPRC and a subset of sporadic papillary renal carcinoma In this study, me screened a large panel of sporadic papillary renal carcinomas and various solid tumors for mutations in the MET protooncogene, Summarizing these and previous results, mutations of the MET proto-oncogene were detected in 17/129 sporadic papillary renal carcinomas but not in other solid tumors. We detected five novel: missense mutations; three of five mutations were located in the ATP-binding region of the tyrosine kinase domain of MET. One novel mutation in MET, V1110I, was located at a codon homologous to an activating mutation in the c-erbB proto-oncogene, These mutations caused constitutive phosphorylation of MET when transfected into NIH3T3 cells. Molecular modeling studies suggest that these activating mutations interfere with the intrasteric mechanism of tyrosine kinase autoinhibition and facilitate transition to the active form of the MET kinase, The low frequency of MET mutations in noninherited papillary renal carcinomas (PRC) suggests that noninherited PRC may develop by a different mechanism than hereditary papillary renal carcinoma. [References: 37]

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