The role of c-Met and VEGFR2 in glioblastoma resistance to bevacizumab

Abstract Dismal prognosis of glioblastoma (GBM) prompts for the identification of response predictors and therapeutic resistance mechanisms of current therapies. The authors investigated the impact of c-Met, HGF, VEGFR2 expression and microvessel density (MVD) in GBM patients submitted to second-lin...

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Autores principales:	Bruno Carvalho, José Manuel Lopes, Roberto Silva, Joana Peixoto, Dina Leitão, Paula Soares, Ana Catarina Fernandes, Paulo Linhares, Rui Vaz, Jorge Lima
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2021
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/8785dff141e34f8482616e3143dc748b
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spelling	oai:doaj.org-article:8785dff141e34f8482616e3143dc748b2021-12-02T17:05:46ZThe role of c-Met and VEGFR2 in glioblastoma resistance to bevacizumab10.1038/s41598-021-85385-12045-2322https://doaj.org/article/8785dff141e34f8482616e3143dc748b2021-03-01T00:00:00Zhttps://doi.org/10.1038/s41598-021-85385-1https://doaj.org/toc/2045-2322Abstract Dismal prognosis of glioblastoma (GBM) prompts for the identification of response predictors and therapeutic resistance mechanisms of current therapies. The authors investigated the impact of c-Met, HGF, VEGFR2 expression and microvessel density (MVD) in GBM patients submitted to second-line chemotherapy with bevacizumab. Immunohistochemical expression of c-Met, HGF, VEGFR2, and MVD was assessed in tumor specimens of GBM patients treated with bevacizumab, after progression under temozolomide. Survival analysis was evaluated according to the expression of the aforementioned biomarkers. c-Met overexpression was associated with a time-to-progression (TTP) after bevacizumab of 3 months (95% CI, 1.5–4.5) compared with a TTP of 7 months (95% CI, 4.6–9.4) in patients with low or no expression of c-Met (p = 0.05). VEGFR2 expression was associated with a TTP after bevacizumab of 3 months (95% CI, 1.8–4.2) compared with a TTP of 7 months (95% CI, 5.7–8.3) in patients with no tumoral expression of VEGFR2 (p = 0.009). Concomitant c-Met/VEGFR2 overexpression was associated with worse overall survival (13 months) compared with concomitant c-Met/VEGFR2 negative expression (19 months; p = 0.025). Our data support the hypothesis that c-Met and VEGFR2 overexpression have a role in the development of glioblastoma early resistance and might predict poorer responses to anti-angiogenic therapies.Bruno CarvalhoJosé Manuel LopesRoberto SilvaJoana PeixotoDina LeitãoPaula SoaresAna Catarina FernandesPaulo LinharesRui VazJorge LimaNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-8 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Bruno Carvalho José Manuel Lopes Roberto Silva Joana Peixoto Dina Leitão Paula Soares Ana Catarina Fernandes Paulo Linhares Rui Vaz Jorge Lima The role of c-Met and VEGFR2 in glioblastoma resistance to bevacizumab
description	Abstract Dismal prognosis of glioblastoma (GBM) prompts for the identification of response predictors and therapeutic resistance mechanisms of current therapies. The authors investigated the impact of c-Met, HGF, VEGFR2 expression and microvessel density (MVD) in GBM patients submitted to second-line chemotherapy with bevacizumab. Immunohistochemical expression of c-Met, HGF, VEGFR2, and MVD was assessed in tumor specimens of GBM patients treated with bevacizumab, after progression under temozolomide. Survival analysis was evaluated according to the expression of the aforementioned biomarkers. c-Met overexpression was associated with a time-to-progression (TTP) after bevacizumab of 3 months (95% CI, 1.5–4.5) compared with a TTP of 7 months (95% CI, 4.6–9.4) in patients with low or no expression of c-Met (p = 0.05). VEGFR2 expression was associated with a TTP after bevacizumab of 3 months (95% CI, 1.8–4.2) compared with a TTP of 7 months (95% CI, 5.7–8.3) in patients with no tumoral expression of VEGFR2 (p = 0.009). Concomitant c-Met/VEGFR2 overexpression was associated with worse overall survival (13 months) compared with concomitant c-Met/VEGFR2 negative expression (19 months; p = 0.025). Our data support the hypothesis that c-Met and VEGFR2 overexpression have a role in the development of glioblastoma early resistance and might predict poorer responses to anti-angiogenic therapies.
format	article
author	Bruno Carvalho José Manuel Lopes Roberto Silva Joana Peixoto Dina Leitão Paula Soares Ana Catarina Fernandes Paulo Linhares Rui Vaz Jorge Lima
author_facet	Bruno Carvalho José Manuel Lopes Roberto Silva Joana Peixoto Dina Leitão Paula Soares Ana Catarina Fernandes Paulo Linhares Rui Vaz Jorge Lima
author_sort	Bruno Carvalho
title	The role of c-Met and VEGFR2 in glioblastoma resistance to bevacizumab
title_short	The role of c-Met and VEGFR2 in glioblastoma resistance to bevacizumab
title_full	The role of c-Met and VEGFR2 in glioblastoma resistance to bevacizumab
title_fullStr	The role of c-Met and VEGFR2 in glioblastoma resistance to bevacizumab
title_full_unstemmed	The role of c-Met and VEGFR2 in glioblastoma resistance to bevacizumab
title_sort	role of c-met and vegfr2 in glioblastoma resistance to bevacizumab
publisher	Nature Portfolio
publishDate	2021
url	https://doaj.org/article/8785dff141e34f8482616e3143dc748b
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The role of c-Met and VEGFR2 in glioblastoma resistance to bevacizumab

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