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Rona S. Carroll, Peter M. Black, Jianping Zhang, Matthias Kirsch, Ivona Percec, Nelson Lau and Abhijit Guha

-horseradish peroxidase detection system. M = meningioma; A431 = human epidermoid carcinoma cell line; EGF-R = epidermal growth factor receptor; EGF-R* = activated epidermal growth factor receptor; Ab:4G10 = anti-phosphotyrosine antibody. Fig. 6. Western blots showing expression and phosphorylation of Shc: immunoprecipitation of 16 meningioma specimen lysates with Ab:Shc and Western blot analysis using Ab:Shc (A) and Ab:4G10 (B). All the meningiomas expressed all three isoforms of Shc, which were also tyrosine phosphorylated (major tyrosine phosphorylation site of Shc

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Walter A. Hall, Marsha J. Merrill, Stuart Walbridge and Richard J. Youle

various human tumor types. Epidermal growth factor receptors have been found on human squamous-cell carcinomas of the lung, breast carcinomas, and glioblastomas multiforme. 7, 12, 15, 22, 28–30, 34, 35 In vitro studies have also shown EGFR's on a variety of tissue-culture cell lines. 13, 15 Transferrin receptors have been found on human breast carcinoma tissue and on a human melanoma cell line. 11, 14, 37 Materials and Methods Tissue Samples Fresh samples of brain-tumor tissue were obtained in the operating room, immediately placed on dry ice, and stored

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Norio Arita, Toru Hayakawa, Shuuichi Izumoto, Takuyu Taki, Takanori Ohnishi, Hiroshi Yamamoto, Shoji Bitoh and Heitaro Mogami

weak + + − 11 67, F rt frontal glioblastoma ++ + − − * Code: ++ = more than 50% of tumor cells are positively stained; + = positive cells are seen scattered in the tissue; weak = few cells are positively stained; − = negative. † Tumor recurrence. Fig. 1. Case 10. Photomicrographs of a glioblastoma section prepared with immunoperoxidase staining with monoclonal anti-epidermal growth factor receptor antibody. Left: The tumor cells at the left are infiltrating into the normal brain at the right, and are

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Uri Tabori, Shlomit Rienstein, Yaara Dromi, Leonor Leider-Trejo, Shlomo Constantini, Yoav Burstein, Rina Dvir, Ninette Amariglio, Amos Toren, Gideon Rechavi, Shai Izraeli and Ayala Aviram

centers will enable us to undertake further comprehensive studies, including RNA extraction for expression of the gene in these rare cases. Epidermal growth factor receptor is an important target for further research because of the small molecules that inhibit this receptor. 20, 28 In the context of disseminated pediatric LGGs, it will probably be better to add these agents as adjuncts to the standard chemotherapy protocols, because current protocols are successful in disease control 19 and because only subsets of the cells express EGFR. Conclusions To our

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Yoshifumi Kawanabe, Tomoh Masaki and Nobuo Hashimoto

: mechanisms of action of calcium antagonists. J Clin Neurosci 1 : 151 – 160 , 1994 Dorsch NWC: A review of cerebral vasospasm in aneurysmal subarachnoid hemorrhage, Part III: mechanisms of action of calcium antagonists. J Clin Neurosci 1: 151–160, 1994 2. Flamant M , Tharaux PL , Placier S , et al : Epidermal growth factor receptor trans -activation mediates the tonic and fibrogenic effects of endothelin in the aortic wall of transgenic mice. FASEB J 17 : 327 – 329 , 2003 Flamant M, Tharaux PL, Placier S

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Hoi Sang U, Olivia D. Espiritu, Patricia Y. Kelley, Melville R. Klauber and James D. Hatton

P rimary human tumors are frequently associated with protooncogene abnormalities, including the deactivation of “tumor suppressor genes” 11, 14, 17, 33–35 or the activation of dominantly acting oncogenes. 2, 8, 19, 24, 40, 46 In the latter situation, structural or numerical alterations lead to enhanced gene expression. The epidermal growth factor receptor (EGFR) gene is the most frequently amplified and overexpressed protooncogene in glioblastomas and is thus implicated in glioma formation. 20, 21, 25, 37, 38, 45 The EGFR gene is also overexpressed in human

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Marc-Eric Halatsch, Esther E. Gehrke, Vassilios I. Vougioukas, Ingolf C. Bötefür, Farhad A.-Borhani, Thomas Efferth, Erich Gebhart, Sebastian Domhof, Ursula Schmidt and Michael Buchfelder

. Ekstrand AJ , Sugawa N , James CD , et al : 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. Proc Natl Acad Sci USA 89 : 4309 – 4313 , 1992 Ekstrand AJ, Sugawa N, James CD, et al: 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. Proc Natl Acad Sci USA 89:4309–4313, 1992 6. Filmus J

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Justin S. Smith, Anita Lal, Miranda Harmon-Smith, Andrew W. Bollen and Michael W. McDermott

cerebral meningiomas. Part 2: In vitro effect of steroids, bromocriptine, and epidermal growth factor on growth of meningiomas . J Neurosurg 73 : 750 – 755 , 1990 2 Andersson U , Guo D , Malmer B , Bergenheim AT , Brannstrom T , Hedman H , : Epidermal growth factor receptor family (EGFR, ErbB2–4) in gliomas and meningiomas . Acta Neuropathol (Berl) 108 : 135 – 142 , 2004 3 Black PM , Carroll R , Glowacka D , Riley K , Dashner K : Platelet-derived growth factor expression and stimulation in human meningiomas . J Neurosurg

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Hoi Sang U, Olivia D. Espiritu, Patricia Y. Kelley, Melville R. Klauber and James D. Hatton

T he epidermal growth factor receptor (EGFR) gene is implicated in glioma genesis because of the high frequency of its overexpression in these tumors. 12, 13, 17, 31, 37 We first investigated whether growth stimulation was the primary role of the EGFR in gliomas because the receptor is intimately associated with growth control in other tumor systems. 2, 3, 5–7, 9, 11, 14, 15, 18, 19, 23, 30, 32, 34–36 Results from this study showed that the EGFR did not appear to mediate solely the growth effects of EGF. We therefore explored the involvement of the EGFR in

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Andreas Waha, Axel Baumann, Helmut K. Wolf, Rolf Fimmers, Jürgen Neumann, Dietmar Kindermann, Kathy Astrahantseff, Ingmar Blümcke, Andreas von Deimling and Uwe Schlegel

M alignant transformation is considered to be the result of a multistep process in which cells acquire mutations of genes that are critical for regulation of cell proliferation and differentiation. 4, 43 In astrocytic gliomas several mutations in such regulatory genes have been identified, some of which are confined to certain grades of malignancy. 8, 9 Amplification and overexpression of the c-erbB gene encoding the epidermal growth factor receptor (EGFR) have been demonstrated in up to 50% of malignant gliomas. 1, 10, 23, 24 The gene product is a 170-kD