Missense mutation of the MET gene detected in human glioma

Young Wan Moon, Robert J. Weil, Svetlana D. Pack, Won Sang Park, Evgenia Pak, Thu Pham, Jayaprakash D. Karkera, Hoon Kyo Kim, Alexander Vortmeyer, Brian G. Fuller, Zhengping Zhuang

Research output: Contribution to journalArticle

21 Citations (Scopus)

Abstract

Multiple mechanisms, such as gene mutations, amplifications, and rearrangements, as well as perturbed mitogen and receptor function, are likely to contribute to glioma formation. The MET (also known as c-met) proto-oncogene located at 7q31-34 has been shown to be amplified in human gliomas, and activating mutations within the tyrosine kinase domain of MET have been causally related to tumorigenesis in hereditary papillary renal cell carcinoma. To elucidate the role of MET gene in glioma formation, sporadic gliomas from 11 patients were examined for MET gene mutations and allelic duplications or deletions by polyermase chain reaction-single strand conformational polymorphism analysis and fluorescence in situ hybridization. Three of 11 sporadic gliomas showed a deletion of one copy of the MET gene, and a specific MET gene missense mutation in the remaining gene copy was detected in one of those tumors. The corresponding sequence in non-tumor DNA was normal in all cases. Three of 11 sporadic gliomas showed duplication of one copy of the MET gene, but none of them contained mutations. One tumor showed MET amplification without mutation. Three showed neither allelic change nor mutation. These data suggest that somatic MET gene mutation may play a role in the development of a subgroup of sporadic gliomas. However, MET mutations appear to be absent in the majority of sporadic gliomas.

Original languageEnglish (US)
Pages (from-to)973-977
Number of pages5
JournalModern Pathology
Volume13
Issue number9
DOIs
StatePublished - Jan 1 2000
Externally publishedYes

Fingerprint

Missense Mutation
Glioma
Mutation
Genes
Mitogen Receptors
Proto-Oncogenes
Gene Rearrangement
Gene Amplification
Fluorescence In Situ Hybridization
Renal Cell Carcinoma
Protein-Tyrosine Kinases
Neoplasms
Carcinogenesis
DNA

Keywords

  • Fluorescence in situ hybridization
  • Glioma
  • MET gene
  • Single strand conformation polymorphism analysis

ASJC Scopus subject areas

  • Pathology and Forensic Medicine

Cite this

Moon, Y. W., Weil, R. J., Pack, S. D., Park, W. S., Pak, E., Pham, T., ... Zhuang, Z. (2000). Missense mutation of the MET gene detected in human glioma. Modern Pathology, 13(9), 973-977. https://doi.org/10.1038/modpathol.3880177

Missense mutation of the MET gene detected in human glioma. / Moon, Young Wan; Weil, Robert J.; Pack, Svetlana D.; Park, Won Sang; Pak, Evgenia; Pham, Thu; Karkera, Jayaprakash D.; Kim, Hoon Kyo; Vortmeyer, Alexander; Fuller, Brian G.; Zhuang, Zhengping.

In: Modern Pathology, Vol. 13, No. 9, 01.01.2000, p. 973-977.

Research output: Contribution to journalArticle

Moon, YW, Weil, RJ, Pack, SD, Park, WS, Pak, E, Pham, T, Karkera, JD, Kim, HK, Vortmeyer, A, Fuller, BG & Zhuang, Z 2000, 'Missense mutation of the MET gene detected in human glioma', Modern Pathology, vol. 13, no. 9, pp. 973-977. https://doi.org/10.1038/modpathol.3880177
Moon YW, Weil RJ, Pack SD, Park WS, Pak E, Pham T et al. Missense mutation of the MET gene detected in human glioma. Modern Pathology. 2000 Jan 1;13(9):973-977. https://doi.org/10.1038/modpathol.3880177
Moon, Young Wan ; Weil, Robert J. ; Pack, Svetlana D. ; Park, Won Sang ; Pak, Evgenia ; Pham, Thu ; Karkera, Jayaprakash D. ; Kim, Hoon Kyo ; Vortmeyer, Alexander ; Fuller, Brian G. ; Zhuang, Zhengping. / Missense mutation of the MET gene detected in human glioma. In: Modern Pathology. 2000 ; Vol. 13, No. 9. pp. 973-977.
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