Glioblastoma resistance to anti-VEGF therapy: Has the challenge been MET?

Joseph H. McCarty

doi:10.1158/1078-0432.CCR-13-0051

Glioblastoma resistance to anti-VEGF therapy: Has the challenge been MET?

Joseph H. McCarty

Research output: Contribution to journal › Article › peer-review

30 Scopus citations

Abstract

In glioblastoma cells the receptor tyrosine kinase c-Met is upregulated in response to bevacizumab and plays an important role in promoting invasion and tumor recurrence. These data support novel links between VEGF-A and hepatocyte growth factor and suggest that c-Met and its signaling effectors may be effective targets for anti-invasive therapies.

Original language	English (US)
Pages (from-to)	1631-1633
Number of pages	3
Journal	Clinical Cancer Research
Volume	19
Issue number	7
DOIs	https://doi.org/10.1158/1078-0432.CCR-13-0051
State	Published - Apr 1 2013

ASJC Scopus subject areas

Oncology
Cancer Research

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10.1158/1078-0432.CCR-13-0051

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title = "Glioblastoma resistance to anti-VEGF therapy: Has the challenge been MET?",

abstract = "In glioblastoma cells the receptor tyrosine kinase c-Met is upregulated in response to bevacizumab and plays an important role in promoting invasion and tumor recurrence. These data support novel links between VEGF-A and hepatocyte growth factor and suggest that c-Met and its signaling effectors may be effective targets for anti-invasive therapies.",

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AB - In glioblastoma cells the receptor tyrosine kinase c-Met is upregulated in response to bevacizumab and plays an important role in promoting invasion and tumor recurrence. These data support novel links between VEGF-A and hepatocyte growth factor and suggest that c-Met and its signaling effectors may be effective targets for anti-invasive therapies.

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Glioblastoma resistance to anti-VEGF therapy: Has the challenge been MET?

Abstract

ASJC Scopus subject areas

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