Distribution of epidermal growth factor receptor protein correlates with gain in chromosome 7 revealed by comparative genomic hybridization after microdissection in glioblastoma multiforme.

作者: Bernd F.M. Romeike , Volker Jung , Wolfgang Feiden , Jean R. Moringlane , Klaus D. Zang

DOI: 10.1078/0344-0338-00056

关键词:

摘要: Summary In a recent study, 23 microdissected areas of 10 glioblastoma multiforme (GBM) were investigated for quantitative genomic aberrations using comparative hybridization (CGH). To validate the chromosomal aberrations, as revealed by CGH after microdissection, parallel tissue sections stained immunohistochemically with an antibody that detects both wild-type epidermal growth factor receptor (EGFR) and deletion mutant form (EGFRvIII). Immunostaining was correlated data chromosome 7, because 7 is most frequently aberrant in GBM (here four tumors), this aberration often indicates abnormality EGFR. Nine nine showed gain or amplification (2 areas) contained EGFR-immunoreactive cells. Only three 14 without cells; eleven immunonegative. Our findings demonstrate strong correlation between immunohistochemistry EGFR copy numbers microdissection multiforme.

参考文章(12)
P. Kleihues, Webster K Cavenee, None, Pathology and genetics of tumours of the nervous system. International Agency for Research on Cancer. ,(2000)
U. Novak, A. W. Burgess, A. H. Kaye, L. T. Malden, Selective amplification of the cytoplasmic domain of the epidermal growth factor receptor gene in glioblastoma multiforme. Cancer Research. ,vol. 48, pp. 2711- 2714 ,(1988)
Tony Hunter, The epidermal growth factor receptor gene and its product. Nature. ,vol. 311, pp. 414- 416 ,(1984) , 10.1038/311414A0
A. J. Wong, J. M. Ruppert, S. H. Bigner, C. H. Grzeschik, P. A. Humphrey, D. S. Bigner, B. Vogelstein, Structural alterations of the epidermal growth factor receptor gene in human gliomas Proceedings of the National Academy of Sciences of the United States of America. ,vol. 89, pp. 2965- 2969 ,(1992) , 10.1073/PNAS.89.7.2965
Towia A. Libermann, Harris R. Nusbaum, Nissim Razon, Richard Kris, Irit Lax, Hermona Soreq, Nigel Whittle, Michael D. Waterfield, Axel Ullrich, Joseph Schlessinger, Amplification, enhanced expression and possible rearrangement of EGF receptor gene in primary human brain tumours of glial origin Nature. ,vol. 313, pp. 144- 147 ,(1985) , 10.1038/313144A0
Volker Jung, Bernd F. M. Romeike, Wolfram Henn, Wolfgang Feiden, Jean R. Moringlane, Klaus D. Zang, Steffi Urbschat, Evidence of Focal Genetic Microheterogeneity in Glioblastoma Multiforme by Area-Specific CGH on Microdissected Tumor Cells Journal of Neuropathology and Experimental Neurology. ,vol. 58, pp. 993- 999 ,(1999) , 10.1097/00005072-199909000-00009
Sandra H. Bigner, Peter C. Burger, Albert J. Wong, Mark H. Werner, Stanley R. Hamilton, Lawrence H. Muhlbaier, Bert Vogelstein, Darell D. Bigner, Gene amplification in malignant human gliomas: clinical and histopathologic aspects. Journal of Neuropathology and Experimental Neurology. ,vol. 47, pp. 191- 205 ,(1988) , 10.1097/00005072-198805000-00001
Kunihiko Watanabe, Osamu Tachibana, Kazufumi Sato, Yasuhiro Yonekawa, Paul Kleihues, Hiroko Ohgaki, None, Overexpression of the EGF Receptor and p53 Mutations are Mutually Exclusive in the Evolution of Primary and Secondary Glioblastomas Brain Pathology. ,vol. 6, pp. 217- 223 ,(1996) , 10.1111/J.1750-3639.1996.TB00848.X
A. J. Ekstrand, N. Sugawa, C. D. James, V. P. Collins, Amplified and rearranged epidermal growth factor receptor genes in human glioblastomas reveal deletions of sequences encoding portions of the N- and/or C-terminal tails. Proceedings of the National Academy of Sciences of the United States of America. ,vol. 89, pp. 4309- 4313 ,(1992) , 10.1073/PNAS.89.10.4309
A. J. Wong, S. H. Bigner, D. D. Bigner, K. W. Kinzler, S. R. Hamilton, B. Vogelstein, Increased expression of the epidermal growth factor receptor gene in malignant gliomas is invariably associated with gene amplification. Proceedings of the National Academy of Sciences of the United States of America. ,vol. 84, pp. 6899- 6903 ,(1987) , 10.1073/PNAS.84.19.6899