Revascularization of ischemic tissues by PlGF treatment, and inhibition of tumor angiogenesis, arthritis and atherosclerosis by anti-Flt1

By A. Luttun, M. Tjwa, L. Moons, Yan Wu, A. Angelillo-Scherrer, F. Liao, J. Nagy, A. Hooper, Josef Priller, Bert De Klerck and 12 more. Nature Medicine, 2002

1,130 citations recorded by the source corpus.

Subfields: Cancer Research, Immunology and Allergy, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/6ebe211c9c537eb3468f5335e26281f570f6ab43

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cancer Research

1. N. Ferrara
2. M. Shibuya
3. R. Kerbel
4. D. Hanahan
5. G. Bergers
6. H. Gerber
7. J. Joyce
8. W. Novotny

In Immunology and Allergy

1. M. Shibuya
2. N. Ferrara
3. G. Bergers
4. D. Hanahan

In Molecular Biology

1. N. Ferrara
2. D. Hanahan
3. R. Kerbel
4. M. Shibuya
5. J. Joyce
6. Rakesh K. Jain
7. D. Hicklin
8. H. Gerber

Citations in the corpus

• Vascular Endothelial Growth Factor and Angiogenesis (2004, background): “A VEGFR-1 antibody has recently been shown to inhibit tumor growth almost as effectively as a VEGFR-2 antibody (Luttun et al., 2002), indicating that the poorly understood VEGFR-1 might be more important than previously thought.”
• Differential roles of vascular endothelial growth factor receptor-1 and receptor-2 in angiogenesis. (2006, background): “On the other hand, VEGFR1-dependent signaling is important for certain tumor angiogenesis and the progression of rheumatoid arthritis and atherosclerosis (Carmeliet et al., 2001; Luttun et al., 2002; Zhao et al., 2004).”
• Vascular endothelial growth factor and its receptor system: physiological functions in angiogenesis and pathological roles in various diseases. (2013, background): “Although the kinase activity of VEGFR-1 is relatively weak compared with that of VEGFR-2, PlGF stimulates survival signals in endothelial cells and promotes angiogenesis without a severe inflammatory response (12).”
• Biology of vascular endothelial growth factors (2006, background): “PlGF-2 overexpression results in the production of significant angiogenesis in different tissues [21,23].”
• VEGF-A stimulates lymphangiogenesis and hemangiogenesis in inflammatory neovascularization via macrophage recruitment. (2004, background): “in the stimulation of pathological HA (51, 52), three facts “argue against” the possibility that endogenous PlGF plays a significant”
• Drug resistance by evasion of antiangiogenic targeting of VEGF signaling in late-stage pancreatic islet tumors. (2005, result): “The results showed that MF1 was active and able to block VEGFR1 function in vivo in the same dosage regimen (Figure S2), consistent with a previous study (Luttun et al., 2002).”
• Excess placental soluble fms-like tyrosine kinase 1 (sFlt1) may contribute to endothelial dysfunction, hypertension, and proteinuria in preeclampsia. (2003, neutral): “This work also has implications for anti-VEGF or anti-PlGF compounds currently undergoing clinical trials for the treatment of cancer and other disorders (19, 47).”
• Angiogenesis as a therapeutic target (2005, background): “However, there is growing evidence that VEGFR-1 has significant roles in haematopoiesis and in the recruitment of monocytes and other bone-marrow-derived cells that may home in on the tumour vasculature and promote angiogenesi”