Alterations affecting the epidermal growth factor/transforming growth factor alpha-responsive mitogenic pathway are frequently detected in malignancies. In particular, the epidermal growth factor receptor has been found overexpressed in a number of human tumors. Production and secretion of transforming growth factor type alpha has also been shown in several tumor cells but not in their normal counterparts. In this review we describe the establishment of in vitro model systems to study the transforming potential of these molecules and summarize our current understanding of the mechanisms involved in transformation by genes encoding a growth factor and a growth factor receptor.

Mechanisms by which EGF receptor and TGF alpha contribute to malignant transformation / E. Di Marco, J. H. Pierce, S. A. Aaronson, P. P. Di Fiore. - In: NATURAL IMMUNITY AND CELL GROWTH REGULATION. - ISSN 0254-7600. - 9:3(1990), pp. 209-21-221.

Mechanisms by which EGF receptor and TGF alpha contribute to malignant transformation

P. P. Di Fiore
Ultimo
1990

Abstract

Alterations affecting the epidermal growth factor/transforming growth factor alpha-responsive mitogenic pathway are frequently detected in malignancies. In particular, the epidermal growth factor receptor has been found overexpressed in a number of human tumors. Production and secretion of transforming growth factor type alpha has also been shown in several tumor cells but not in their normal counterparts. In this review we describe the establishment of in vitro model systems to study the transforming potential of these molecules and summarize our current understanding of the mechanisms involved in transformation by genes encoding a growth factor and a growth factor receptor.
Gene Expression Regulation, Neoplastic; Animals; Oncogenes; Transfection; Receptor, Epidermal Growth Factor; Humans; Transforming Growth Factors; Cell Transformation, Neoplastic; Cell Line; Cell Division
Settore MED/04 - Patologia Generale
1990
Article (author)
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2434/195752
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