Cuiling Zhong

TL;DR: In this article, the authors investigated cellular and molecular events that mediate refractoriness of tumors to anti-angiogenic therapy and found that anti-VEGF refractiness is associated with infiltration of the tumor tissue by CD11b+Gr1+ myeloid cells.

TL;DR: Findings indicate that, in models, refractoriness to anti-VEGF treatment is determined by the ability of tumors to prime and recruit CD11b+Gr1+ cells.

TL;DR: C3 transferase, an inhibitor of the low molecular weight GTP-binding protein Rho, blocks the binding of fibronectin and the 70-kD NH2-terminal fibronECTin fragment to cells and blocks the assembly of fibronsectin into matrix induced by serum or lysophosphatidic acid, providing evidence that self-assembly sites within fibronctin are exposed by tension.

TL;DR: Bv8 modulates mobilization of CD11b+Gr1+ cells from the bone marrow during tumour development and also promotes angiogenesis locally, which is additive to those of anti-Vegf antibodies or cytotoxic chemotherapy.

TL;DR: It is shown that platelet-derived growth factor C (PDGF-C) is upregulated in TAFs from resistant tumors and suggested that some tumors may overcome inhibition of VEGF-mediated angiogenesis through upregulation of PDGF- C.