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Titlebook: EGF Receptor in Tumor Growth and Progression; R. B. Lichtner,R. N. Harkins Conference proceedings 1997 Springer-Verlag Berlin Heidelberg 1

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EGF Receptor Inhibition by Antibody as Anticancer Therapy,ainsbury et al. 1985; Harris et al. 1989), and lung (Veale et al. 1987; Hendler et al. 1989). Furthermore, EGF receptor activation has been implicated in autocrine stimulation of cell growth in many experimental studies (Mendelsohn 1990). Therefore, the EGF receptor appears to be an excellent target for antitumor therapy (Mendelsohn 1989).
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A Difference That Makes No Difference,aselga and Mendelsohn 1994; Eccles et al. 1995). The cell surface location of these molecules renders them attractive targets for a variety of immunotherapeutic strategies, some of which are showing promise in preclinical and early clinical trials.
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The Role of Epidermal Growth Factor Receptor in the Initiation and Progression of Malignancy,actically demonstrated in the case of avian erythroblastosis by functional replacement of v-erbB through human EGFR (Khazaie et al. 1988). Oncogenes and deregulation of cell proliferation provided a powerful tool for explaining cancer at the molecular level (Sinn et al. 1987).
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Preclinical Studies with Human Tumour Xenografts Using Rat Monoclonal Antibodies Directed Against taselga and Mendelsohn 1994; Eccles et al. 1995). The cell surface location of these molecules renders them attractive targets for a variety of immunotherapeutic strategies, some of which are showing promise in preclinical and early clinical trials.
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Michal Borkovec,Ger J. M. Koperst studied receptor signaling systems from this family is the epidermal growth factor receptor (EGFR). The EGFR is widely expressed in mammals and has been implicated in various stages of embryonic development. Recently, EGFR knockout mice by targeted disruption of exon 1 (Sibilia and Wagner 1995) o
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iple tyrosine residues. This process, commonly designated as “autophosphorylation” is the initial and a crucial event of growth factor signaling, which is followed by initiation of a multitude of downstream signaling chains (Ullrich and Schlessinger 1990; Fantl et al. 1993). RTK autophosphorylation
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Phase-transfer catalyzed reactions,crophages (Besner et al. 1990) and subsequently cloned and sequenced from the human macrophage-like cell line U-937 (Higashiyama et al. 1991). HB-EGF was considered to be a member of the family of EGF-like growth factors based on its primary structure containing six conserved cysteine residues (Higa
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