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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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书目名称EGF Receptor in Tumor Growth and Progression
编辑R. B. Lichtner,R. N. Harkins
视频video
丛书名称Ernst Schering Foundation Symposium Proceedings
图书封面Titlebook: EGF Receptor in Tumor Growth and Progression;  R. B. Lichtner,R. N. Harkins Conference proceedings 1997 Springer-Verlag Berlin Heidelberg 1
描述The last 15 years have brought an understanding of growth and differentiation at the molecular level, expanding our knowledge of the origin and progression of cancer. Early breakthroughs defining growth control pathways came via studies of oncogenes, mutated signaling molecules that have lost the capacity to tum off their proliferative signal. Oncogenes with diverse growth-promoting activities have been discovered, covering the gamut from cell surface to nuclear signaling. Sequencing of these oncogenes revealed that they were mutated forms of captured cellular genes and displayed tyrosine kinase activity. The epidermal growth factor (EGF) receptor was the first of 40-50 transmembrane tyrosine kinase receptors to be cloned and sequenced. Beyond cell proliferation, activation of EGF receptor by its specific ligands controls important physiological processes, such as cell differentiation, apoptosis, cell migration, and cell shape. Activation of autocrine growth loops, consisting in solid human tumors of upregulated expression of EGFR together with increased production of ligands suggested its crucial role in autonomous tumor growth.
出版日期Conference proceedings 1997
关键词EGF Receptor; EGF Rezeptor; Signal Transduction; Signaltransduktion; Tyrosinkinase; angiogenesis; antibody
版次1
doihttps://doi.org/10.1007/978-3-662-03391-3
isbn_softcover978-3-662-03393-7
isbn_ebook978-3-662-03391-3Series ISSN 0947-6075
issn_series 0947-6075
copyrightSpringer-Verlag Berlin Heidelberg 1997
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Epidermal Growth Factor Receptor Expression in Head and Neck Tumorigenesis and Saturation of EGFR wrials is the understanding that the whole epithelial lining of the tract shares a common carcinogenic exposure, resulting in an increased cancer risk throughout the exposed epithelum. This entire epithelium was first described as “condemned mucosa” associated with “field cancerization” by Slaughter
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The Role of Estrogen in the Regulation of EGFR Expression,987). Moreover, many cell regulators such as EGF, 12-O-tetradecanoyl phorbol acetate (TPA), and sodium butyrate have opposite effects on the expression of the two receptors (Lee et al. 1989; Secada et al. 1991; De Fazio et al. 1992). This well-established inverse correlation between EGFR and ER expr
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Conference proceedings 1997poptosis, cell migration, and cell shape. Activation of autocrine growth loops, consisting in solid human tumors of upregulated expression of EGFR together with increased production of ligands suggested its crucial role in autonomous tumor growth.
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0947-6075 tiation, apoptosis, cell migration, and cell shape. Activation of autocrine growth loops, consisting in solid human tumors of upregulated expression of EGFR together with increased production of ligands suggested its crucial role in autonomous tumor growth.978-3-662-03393-7978-3-662-03391-3Series ISSN 0947-6075
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Michal Borkovec,Ger J. M. Koperts with transgenic mice suggest that an autocrine mechanism involving the EGFR could be expected to play a role in the initiation and/or progression of tumors. Transgenic mice expressing transforming growth factor-α (TGF-α) were reported to develop mammary and hepatocellular carcinoma as well as pan
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ptide substrate and the ATP binding sites. In the phosphorylated form it is expected to become disengaged from the active center and to allow access of the substrates. In terms of homology it is possible that such a mechanism might operate similarly in other RTK. (2) Autophosphorylation creates bind
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