Por favor, use este identificador para citar o enlazar este ítem: http://hdl.handle.net/10201/18810

Título: Elimination of transformed cells by normal cells: a novel concept for the control of carcinogenesis
Fecha de publicación: 1996
Editorial: Murcia : F. Hernández
ISSN: 0213-3911
Materias relacionadas: CDU::6 - Ciencias aplicadas::61 - Medicina::616 - Patología. Medicina clínica. Oncología
Palabras clave: Apoptosis
Carcinogenesis
Resumen: Control of transformed cells by neighbouring normal cells is known since the beginning of transformation studies in vitro. The classical explanation for this phenomenon is based on proliferation inhibition of transformed cells by normal cells. We extend this model by presenting data that show that TGF-B-treated normal cells can eliminate transformed cells by induction of apoptosis. Both the TGF-8-induced signal pathway in normal cells, leading to the production of a short-lived apoptosis-inducing factor, as well as the specific interaction of this factor with transformed cells depend on the action of reactive oxygen species. Sensitivity to induction of apoptosis seems to be a common feature associated with the transformed state, independent of the originally transforming principle. Therefore, tumor development should require either interference with the process of elimination or acquisition of resistance against it. We discuss experimental evidence for interfering substances, such as antioxidants, as well as for genetic systems that protect transformed cells from the negative effects of their cellular environment, such as Bcl-2 or papilloma viruses. These findings, as well as the general resistance of exvivo tumor cells against induction of apoptosis are in line with the novel model of control of tumor progression presented by us in this review.
Autor/es principal/es: Bauer, G.
Publicado en: Histology and histopathology
URI: http://hdl.handle.net/10201/18810
Tipo de documento: info:eu-repo/semantics/article
Número páginas / Extensión: 19
Derechos: info:eu-repo/semantics/openAccess
Aparece en las colecciones:Vol.11, nº 1 (1996)

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