Topic
Angiogenesis
About: Angiogenesis is a research topic. Over the lifetime, 58248 publications have been published within this topic receiving 3290129 citations. The topic is also known as: blood vessel formation from pre-existing blood vessels & GO:0001525.
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TL;DR: The function of vascular endothelial growth factor in cancer is not limited to angiogenesis and vascular permeability, and the neuropilins are crucial for mediating the effects of VEGF on tumour cells, primarily because of their ability to regulate the function and the trafficking of growth factor receptors and integrins.
Abstract: The function of vascular endothelial growth factor (VEGF) in cancer is not limited to angiogenesis and vascular permeability. VEGF-mediated signalling occurs in tumour cells, and this signalling contributes to key aspects of tumorigenesis, including the function of cancer stem cells and tumour initiation. In addition to VEGF receptor tyrosine kinases, the neuropilins are crucial for mediating the effects of VEGF on tumour cells, primarily because of their ability to regulate the function and the trafficking of growth factor receptors and integrins. This has important implications for our understanding of tumour biology and for the development of more effective therapeutic approaches.
989 citations
TL;DR: A vascular growth factor whose primary role is in postnatal angiogenic remodeling is defined and it is demonstrated that members of the VEGF and Angiopoietin families collaborate during development of the lymphatic vasculature.
988 citations
TL;DR: Several recent studies have identified nuclear factor-κB as a key modulator in driving inflammation to cancers, and other proteins with extensive roles in inflammation and cancer, such as signal transducers and activators of transcription, Nrf2, and nuclear factor of activated T cells, are proposed to be promising targets for future studies.
Abstract: Several recent studies have identified nuclear factor-κB as a key modulator in driving inflammation to cancers. Besides this transcription factor, essential in regulating inflammation and cancer development, an inflammatory microenvironment inhabiting various inflammatory cells and a network of signaling molecules are also indispensable for the malignant progression of transformed cells, which is attributed to the mutagenic predisposition of persistent infection-fighting agents at sites of chronic inflammation. As a subverted host response to inflammation-induced tumors, the inflammatory cells and regulators may facilitate angiogenesis and promote the growth, invasion, and metastasis of tumor cells. Thus far, research regarding inflammation-associated cancer development has focused on cytokines and chemokines as well as their downstream targets in linking inflammation and cancer. Moreover, other proteins with extensive roles in inflammation and cancer, such as signal transducers and activators of transcription, Nrf2, and nuclear factor of activated T cells, are also proposed to be promising targets for future studies. The elucidation of their specific effects and interactions will accelerate the development of novel therapeutic interventions against cancer development triggered by inflammation. (Mol Cancer Res 2006;4(4):221–33)
987 citations
TL;DR: The VEGF/VPF ligands and receptors are crucial regulators of vasculogenesis, angiogenesis, lymphangiogenesis and vascular permeability in vertebrates and mapping the signaling system of these important receptors may provide the knowledge necessary to suppress specific signaling pathways in major human diseases.
985 citations
TL;DR: The approaches to inhibittumor angiogenesis and edema formation in glioblastoma patients will concentrate on the disruption of VEGF/VEGF receptorsignal transduction pathway in vivo.
Abstract: Vascular endothelial growth factor (VEGF) is a hypoxia-inducible angiogenesis and vascular permeability factor which is expressed in high amounts in perinecrotic palisading cells in human glioblastomas. In vitro VEGF gene expression is enhanced approximately ten times by hypoxia. Current evidence suggests, that hypoxia is also the driving force for VEGF gene expression in glioblastoma cells in vivo and represents the most important trigger for tumor angiogenesis and edema. Our approaches to inhibit tumor angiogenesis and edema formation in glioblastoma patients will concentrate on the disruption of VEGF/VEGF receptor signal transduction pathway in vivo.
982 citations