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Anti-VEGF antibody in experimental hepatoblastoma: suppression of tumor growth and altered angiogenesis.

Abstract：

BACKGROUND:Hepatoblastoma is the most common primary hepatic malignancy of childhood, frequently presenting as advanced disease. Vascular endothelial growth factor (VEGF) is an endothelial mitogen and survival factor critical to growth and angiogenesis in many human cancers. Inhibition of VEGF effectively suppresses tumorigenesis in multiple experimental models. The authors hypothesized that anti-VEGF antibody would alter vascular architecture and impede tumor growth in experimental hepatoblastoma. METHODS:The Institutional Animal Care and Use Committee of Columbia University approved all protocols. Xenografts were established in athymic mice by intrarenal injection of cultured human hepatoblastoma cells. Anti-VEGF antibody (100 microg/dose) or vehicle was administered intraperitoneally 2 times per week for 5 weeks. At week 6, 10 control/treated mice were killed and remaining animals maintained without treatment until week 8. Tumor weights were compared by Kruskal-Wallis analysis, and vascular alterations ascertained by fluorescein angiography and specific immunostaining. RESULTS:Anti-VEGF antibody significantly inhibited tumor growth at 6 weeks (1.85 g +/- 0.60 control, 0.05 +/- 0.03 antibody, P <.0003). In comparison with controls, treated xenografts showed decreased vascularity and dilated surviving vessels with prominent vascular smooth muscle elements. CONCLUSIONS:Specific anti-VEGF therapy inhibits neoangiogenesis and significantly suppresses tumor growth in experimental hepatoblastoma. Surviving vasculature displays dilation and increased vascular smooth muscle. Anti-VEGF agents may represent new therapeutic alternatives for children with advanced disease.

journal_name

J Pediatr Surg

journal_title

Journal of pediatric surgery

authors

McCrudden KW,Hopkins B,Frischer J,Novikov A,Huang J,Kadenhe A,New T,Yokoi A,Yamashiro DJ,Kandel JJ,Middlesworth W

doi

10.1053/jpsu.2003.50099

subject

Has Abstract

pub_date

2003-03-01 00:00:00

pages

308-14; discussion 308-14

issue

3

eissn

0022-3468

issn

1531-5037

pii

S0022346802631070

journal_volume

38

pub_type

杂志文章

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