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Tumor refractoriness to anti-VEGF treatment is mediated by CD11b+Gr1+ myeloid cells.

Abstract：

:Vascular endothelial growth factor (VEGF) is an essential regulator of normal and abnormal blood vessel growth. A monoclonal antibody (mAb) that targets VEGF suppresses tumor growth in murine cancer models and human patients. We investigated cellular and molecular events that mediate refractoriness of tumors to anti-angiogenic therapy. Inherent anti-VEGF refractoriness is associated with infiltration of the tumor tissue by CD11b+Gr1+ myeloid cells. Recruitment of these myeloid cells is also sufficient to confer refractoriness. Combining anti-VEGF treatment with a mAb that targets myeloid cells inhibits growth of refractory tumors more effectively than anti-VEGF alone. Gene expression analysis in CD11b+Gr1+ cells isolated from the bone marrow of mice bearing refractory tumors reveals higher expression of a distinct set of genes known to be implicated in active mobilization and recruitment of myeloid cells. These findings indicate that, in our models, refractoriness to anti-VEGF treatment is determined by the ability of tumors to prime and recruit CD11b+Gr1+ cells.

journal_name

Nat Biotechnol

journal_title

Nature biotechnology

authors

Shojaei F,Wu X,Malik AK,Zhong C,Baldwin ME,Schanz S,Fuh G,Gerber HP,Ferrara N

doi

10.1038/nbt1323

subject

Has Abstract

pub_date

2007-08-01 00:00:00

pages

911-20

issue

8

eissn

1087-0156

issn

1546-1696

pii

nbt1323

journal_volume

25

pub_type

杂志文章

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