Fang Chen

TL;DR: In murine tumor models, administration of sunitinib markedly reduced chemotherapy-induced bone marrow toxicity and VEGF increased chemotoxicity by synergistically suppressing bone marrow hematopoiesis with cytostatic drugs, shedding light on molecular mechanisms by which ADs in combination with chemotherapy produce survival benefits.

TL;DR: It is demonstrated that vascular dilation through the VEGFR2 signaling is the mechanism underlying VEGF-induced BM mobilization and anemia and have therapeutic implications by targeting VEGfr2 for cancer therapy.

TL;DR: In a mouse tumor model, tumor-derived VEGF acts as an endocrine-like hormone to induce extramedullary hematopoiesis by targeting distal organs in the host by altering angiogenic profiles, which sheds new light on complex biological functions of V EGF.

TL;DR: It is shown discontinuation of anti-VEGF treatment creates a time-window of profound structural changes of liver sinusoidal vasculatures, exhibiting hyper-permeability and enlarged open-pore sizes of the fenestrated endothelium and loss of VE-cadherin.