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Fighting vessel dysmorphia to improve glioma chemotherapy

High‐grade gliomas are aggressive and abundantly vascular tumors, and as in most cancer types, blood vessels in advanced lesions are highly abnormal. Poor perfusion and vascular leakage in tumor tissue resulting in hypoxia, necrosis, and high interstitial fluid pressure can hamper the efficient deli...

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Detalles Bibliográficos
Autores principales: Lohela, Marja, Alitalo, Kari
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5709761/
https://www.ncbi.nlm.nih.gov/pubmed/29127101
http://dx.doi.org/10.15252/emmm.201708431
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author Lohela, Marja
Alitalo, Kari
author_facet Lohela, Marja
Alitalo, Kari
author_sort Lohela, Marja
collection PubMed
description High‐grade gliomas are aggressive and abundantly vascular tumors, and as in most cancer types, blood vessels in advanced lesions are highly abnormal. Poor perfusion and vascular leakage in tumor tissue resulting in hypoxia, necrosis, and high interstitial fluid pressure can hamper the efficient delivery of chemotherapy. Tumor angiogenesis is known to be supported by host leukocytes recruited to the tumor microenvironment, but the mechanisms leading to dysfunctional vascular network formation are incompletely understood. In this issue of EMBO Molecular Medicine, Mathivet et al (2017) present an elegant study, where longitudinal intravital imaging gives new insight on how recruitment and polarization of tumor‐associated macrophages regulate aberrant angiogenesis in experimental gliomas. They show that macrophage targeting results in vessel normalization and improved chemotherapy response, suggesting that the combination of these therapeutic modalities could improve the outcome of glioma treatment in the clinic.
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spelling pubmed-57097612017-12-06 Fighting vessel dysmorphia to improve glioma chemotherapy Lohela, Marja Alitalo, Kari EMBO Mol Med News & Views High‐grade gliomas are aggressive and abundantly vascular tumors, and as in most cancer types, blood vessels in advanced lesions are highly abnormal. Poor perfusion and vascular leakage in tumor tissue resulting in hypoxia, necrosis, and high interstitial fluid pressure can hamper the efficient delivery of chemotherapy. Tumor angiogenesis is known to be supported by host leukocytes recruited to the tumor microenvironment, but the mechanisms leading to dysfunctional vascular network formation are incompletely understood. In this issue of EMBO Molecular Medicine, Mathivet et al (2017) present an elegant study, where longitudinal intravital imaging gives new insight on how recruitment and polarization of tumor‐associated macrophages regulate aberrant angiogenesis in experimental gliomas. They show that macrophage targeting results in vessel normalization and improved chemotherapy response, suggesting that the combination of these therapeutic modalities could improve the outcome of glioma treatment in the clinic. John Wiley and Sons Inc. 2017-11-10 2017-12 /pmc/articles/PMC5709761/ /pubmed/29127101 http://dx.doi.org/10.15252/emmm.201708431 Text en © 2017 The Authors. Published under the terms of the CC BY 4.0 license This is an open access article under the terms of the Creative Commons Attribution 4.0 (http://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle News & Views
Lohela, Marja
Alitalo, Kari
Fighting vessel dysmorphia to improve glioma chemotherapy
title Fighting vessel dysmorphia to improve glioma chemotherapy
title_full Fighting vessel dysmorphia to improve glioma chemotherapy
title_fullStr Fighting vessel dysmorphia to improve glioma chemotherapy
title_full_unstemmed Fighting vessel dysmorphia to improve glioma chemotherapy
title_short Fighting vessel dysmorphia to improve glioma chemotherapy
title_sort fighting vessel dysmorphia to improve glioma chemotherapy
topic News & Views
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5709761/
https://www.ncbi.nlm.nih.gov/pubmed/29127101
http://dx.doi.org/10.15252/emmm.201708431
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