Anti-PlGF inhibits growth of VEGF(R)-inhibitor-resistant tumors without affecting healthy vessels.

By C. Fischer, B. Jonckx, M. Mazzone, S. Zacchigna, S. Loges, Lucia Pattarini, E. Chorianopoulos, L. Liesenborghs, Marta Koch, M. de Mol and 10 more. Cell, 2007

805 citations recorded by the source corpus.

Subfields: Cancer Research, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/a5df7d7fba894cf518a2c95a174f005e28740ea0

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Citations in the corpus

Cancer-related inflammation (2008, background): “The pro-angiogenic protein vascular endothelial growth factor (VEGF) and related molecules are potent monocyte attractants and contribute to the recruitment of monocytes into primary tumours and the metastatic nich”
Anti-angiogenic therapy for cancer: current progress, unresolved questions and future directions (2014, background): “Combined inhibition of VEGF and PLGF was shown to be more effective at suppressing primary tumour growth than VEGF inhibition alone in several preclinical models [26, 234].”
Targeting the tumour vasculature: insights from physiological angiogenesis (2010, background): “The function of PLGF, despite its name, is unclear during placentation, and further elucidation of its function might help us to understand why its expression is increased in certain pathological state”
VEGF in Signaling and Disease: Beyond Discovery and Development (2019, background): “The role of PlGF in angiogenesis and its significance as a therapeutic target remained largely unclear, with conflicting reports on the effects of antiPlGF antibodies on tumor angiogenesis and growth (Bais et al., 2010; Fischer et al., 2007).”
The role of myeloid cells in the promotion of tumour angiogenesis (2008, background): “Increased levels of other monocyte-attracting chemokines such as placental growth factor (PlGF, PGF”
Accessories to the crime: functions of cells recruited to the tumor microenvironment. (2012, positive): “Similarly, TAM production of the VEGF family member PIGF stimulates angiogenesis in some tumors (Rolny et al., 2011) and thus TAMs may present a mechanism for acquiring resistance to anti-VEGF-A/VEGFR therapies (Fischer et al., 2007; Motzer et al., 2006; Willett et al., 2005).”
PDGF-C mediates the angiogenic and tumorigenic properties of fibroblasts associated with tumors refractory to anti-VEGF treatment. (2009, background): “Other studies investigating tumor resistance/refractoriness to antiangiogenic therapies with VEGF blockers have identified additional potential mechanisms, including expression of alternative angiogenic factors (Bergers and Hanahan, 2008; Fischer et al., 2007), selection of hypoxia-resistant tumor c”
Ten years of anti-vascular endothelial growth factor therapy (2016, background): “Indeed, the role of PlGF in tumour angiogenesis and its significance as a therapeutic target remain controversial 140,141 .”
HRG inhibits tumor growth and metastasis by inducing macrophage polarization and vessel normalization through downregulation of PlGF. (2011, methodology): “, 2004); RT-PCR was described (Fischer et al., 2007).”