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The main problem in the development of antiangiogenic agents is that multiple angiogenic molecules may be produced by tumors, and tumors at different stages of development may depend on different angiogenic factors for their blood supply.
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Newer treatment strategies have focused on molecules that inhibit multiple angiogenic pathways involved in the development and progession of tumors.
Angiogenesis, the formation of new vessels, is found in Multiple Sclerosis (MS) demyelinating lesions following Vascular Endothelial Growth Factor (VEGF) release and the production of several other angiogenic molecules.
Abnormal activation of FoxM1 leads to overexpression of multiple angiogenic genes, such as MMP-2, Cav-1, ZEB1 and ZEB2, which result in overexpression of multiple pro-invasion and -metastasis molecules [ 28, 33– 33].
This result indicates that fullerene-containing materials serve as a potent antiangiogenesis inhibitor that can simultaneously target multiple angiogenic factors.
The angiogenesis is a co-ordinated process that requires the participation of multiple angiogenic factors.
Therefore the existence of angiogenic molecules and the density of activated endothelial cells in individual tumours is of major interest.
We found that cadmium altered the mRNA expression of the two important angiogenic molecules VEGF-A and PLGF.
This avascular phenotype was mediated by inhibition of angiogenic molecules.
This effect is mediated by inhibiting angiogenic molecules (Ang-1, Ang-2 and VEGF).
However, the benefits of anti-angiogenic therapy can be limited by redundant mechanisms of angiogenesis control, a problem that may potentially be overcome by targeting multiple angiogenic pathways or the use of broad spectrum angiogenic inhibitors [6].
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