In 1971, J. Folkman published in the “New England Journal of Medicine” a hypothesis that tumor growth is angiogenesis-dependent. Folkman introduced the concept that tumors probably secrete diffusible molecules that could stimulate the growth of new blood vessels toward the tumor and that the resulting tumor neovascularization could conceivably be prevented or interrupted by angiogenesisinhibitors. Solid and haematological tumors consist of an avascular and a subsequent vascular phase. Assuming that this depends on the release of angiogenic factors, acquisition of angiogenic capability can be seen as an expression of progression from neoplastic transformation to tumor growth and metastasis. Beginning in the 1980’s, the biopharmaceutical industry began exploiting the field of antiangiogenesis for creating new therapeutic compounds for modulating new blood vessels in tumor growth. INDICE: From the contents 1: 1.1 Early evidence of the vascular phase and its importance in tumor growth. 1.2 Early evidence of tumor cells releasing specific growth factors for blood vessels. 1.3 Tumors in isolated perfused organs: absence of angiogenesis. 1.4 The avascular and the vascular phases of solidtumor growth. 2: 2.1 Isolation of the first angiogenic tumor factor. 2.2 The discovery of basic fibroblast growth factor/fibroblast growth factor-2. 2.3 The discovery of vascular permeability factor/vascular endothelial growth factor. 2.4 The discovery of angiopoietins. 3: 3.1 How do tumor cells switch to the angiogenic phenotype ? 3.2 The concept of angiogenic switch. 3.3 Factors involved in the angiogenic switch. 3.4 What is the evidence that genetic instability promotes the angiogenic switch ? 4: 4.1 Tumor endothelial cells features. 4.2 Tumor basement membrane. 4.3 Tumor pericytes. 5: 5.1 Tumor lymphangiogenesis. 6: 6.1 The contribution of inflammatory cells to tumor angiogenesis.
- ISBN: 978-1-4020-9559-7
- Editorial: Springer
- Encuadernacion: Cartoné
- Páginas: 126
- Fecha Publicación: 01/02/2009
- Nº Volúmenes: 1
- Idioma: Inglés