VEGF and the quest for tumour angiogenesis factors

By N. Ferrara. Nature Reviews. Cancer, 2002

1,434 citations recorded by the source corpus.

Subfields: Cancer Research, Cellular and Molecular Neuroscience, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/14467f8b3003bb52572f653ddfa9dd257957c914

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Citations in the corpus

VEGF-A induces tumor and sentinel lymph node lymphangiogenesis and promotes lymphatic metastasis (2005, background): “Indeed, a large number of studies showed that overexpression of VEGF-A in tumor xenotransplants promotes tumor angiogenesis (30), and that systemic inhibition of VEGF-A, VEGFR-1, or VEGFR-2 inhibits tumor growth and angiogenesis in experimental mouse tumor models and in human cancers (30–32).”
Discovery and development of bevacizumab, an anti-VEGF antibody for treating cancer (2004, background): “The binding specificity of the VEGF-trap is expected to be similar to that of Flt(1-3)IgG because domain 3 of VEGFR2 is insufficient to confer VEGFR2-specific binding(125,126).”
Angiogenesis as a therapeutic target (2005, background): “They suggested that a key aspect of the cancer process is a disease of the vasculature in the whole area affected (reviewed in ref”
The biology of VEGF and its receptors (2003, background): “For over a decade, the role of VEGF (also referred to as VEGFA) in the regulation of angiogenesis was the object of intense investigation (see ref”
Ten years of anti-vascular endothelial growth factor therapy (2016, background): “The first description of a link between human tumours and their blood supply occurred more than 100 years ago 2 , but it was only in 1939 that tumour cells themselves were hypothesized to release a blood vessel growth stimulating factor (REF.”
ANTIANGIOGENESIS STRATEGIES REVISITED: FROM STARVING TUMORS TO ALLEVIATING HYPOXIA (2014, positive): “This discovery propelled the development of both small (e.g., tyrosine kinase inhibitors [TKIs] and peptides] and large molecular weight (e.g., antibodies and receptor bodies) inhibitors of VEGF or its downstream signaling (Ferrara, 2002).”
Angiogenic synergism, vascular stability and improvement of hind-limb ischemia by a combination of PDGF-BB and FGF-2 (2003, background): “FGF-2 and VEGF are potent angiogenic factors in vivo and PDGF-BB has a substantial role in the stabilization of newly formed blood vessel”
AZD2171: a highly potent, orally bioavailable, vascular endothelial growth factor receptor-2 tyrosine kinase inhibitor for the treatment of cancer. (2005, background): “Vascular endothelial growth factor-A (VEGF) is a pivotal stimulus of physiologic and pathologic angiogenesis, including the sustained neovascularization required to support solid tumor growth (1).”
Shared Risk Factors in Cardiovascular Disease and Cancer (2016, background): “new blood-vessel formation, is also evident in hypertensive subjects.(54,55) Several studies suggest that angiotensin II, a key”
The discovery of receptor tyrosine kinases: targets for cancer therapy (2004, background): “VEGF and its receptors are known to have important functions in the regulation of tumour angiogenesi”