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Título: | Interleukin-7 (IL-7) and IL-7 receptor (IL-7R) signalling complex in human solid tumours |
Fecha de publicación: | 2003 |
Editorial: | Murcia : F. Hernández |
ISSN: | 0213-3911 |
Materias relacionadas: | CDU::6 - Ciencias aplicadas::61 - Medicina::616 - Patología. Medicina clínica. Oncología |
Palabras clave: | Lymphangiogenesis Breast cancer |
Resumen: | Interleukin-7 (IL-7) plays an important role in the normal development and maintenance of the human immune system. Its effects are mediated via its receptor, IL-7R. Ligand-receptor engagement results in a cascade of phosphorylation events mediated by various molecules including the Janus kinases (Jak1 and Jak3), PI3-kinase, Stats (signal transducers and activators of transcription) and other molecules. The activation of IL- 7 signalling pathway results in survival, proliferation, differentiation and maturation of haematopoietic cells including B and T lymphocytes. Although the relationship of IL-7 with the development and differentiation of some haematological cancers like leukaemias and lymphomas is well recognised, little is known about it involvement with solid tumours. There are several studies that have revealed IL-7/IL-7R expression in epithelial systems and some human solid epithelial tumours. Furthermore, IL-7 can be produced by some human tumour cells and involved in tumour development and progression. In this review article we have summarised the main biological activities of IL-7 and its downstream signalling complex in relation to some human solid malignancies. |
Autor/es principal/es: | Al-Rawi, M.A.A. Mansel, R.E. Jiang, W.G. |
Forma parte de: | Histology and histopathology |
URI: | http://hdl.handle.net/10201/21452 |
Tipo de documento: | info:eu-repo/semantics/article |
Número páginas / Extensión: | 13 |
Derechos: | info:eu-repo/semantics/openAccess |
Aparece en las colecciones: | Vol.18, nº 3 (2003) |
Ficheros en este ítem:
Fichero | Descripción | Tamaño | Formato | |
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Interleukin7 IL7 and IL7 receptor IL7R.pdf | 386,92 kB | Adobe PDF | ![]() Visualizar/Abrir |
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