Beyond VEGF: Inhibition of the Fibroblast Growth Factor Pathway and Antiangiogenesis

被引：239

作者：

Lieu, Christopher ^{[1
]}

Heymach, John ^{[2
]}

Overman, Michael ^{[1
]}

Tran, Hai ^{[2
]}

Kopetz, Scott ^{[1
]}

机构：

[1] Univ Texas MD Anderson Canc Ctr, Dept Gastrointestinal Med Oncol, Houston, TX 77030 USA

[2] Univ Texas MD Anderson Canc Ctr, Dept Thorac Head & Neck Med Oncol, Houston, TX 77030 USA

来源：

CLINICAL CANCER RESEARCH | 2011年 / 17卷 / 19期

关键词：

TYROSINE KINASE INHIBITOR; FGF-BINDING PROTEIN; CELL-ADHESION; PHASE-I; ANGIOGENIC FACTORS; COLORECTAL-CANCER; BREAST-CANCER; FACTOR RECEPTOR-3; HEPARAN-SULFATE; MESSENGER-RNA;

D O I：

10.1158/1078-0432.CCR-11-0659

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Fibroblast growth factor (FGF) signaling regulates cell proliferation, differentiation, survival, angiogenesis, and wound healing. Compelling evidence for deregulated FGF signaling in tumorigenesis continues to emerge, and a growing body of research suggests that FGF may also play an integral role in the resistance to anti-VEGF therapy. Although agents targeting FGF signaling are early in development, the potential to target both the VEGF and FGF pathways may translate into improvements in the clinical care of cancer patients. Clin Cancer Res; 17(19); 6130-9. (C) 2011 AACR.

引用

页码：6130 / 6139

页数：10

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