دورية أكاديمية

Intratumoral VEGF nanotrapper reduces gliobastoma vascularization and tumor cell mass.

التفاصيل البيبلوغرافية
العنوان: Intratumoral VEGF nanotrapper reduces gliobastoma vascularization and tumor cell mass.
المؤلفون: Sousa F; i3S - Instituto de Investigação e Inovação em Saúde, Universidade do Porto, Rua Alfredo Allen 208, 4200-393 Porto, Portugal; INEB - Instituto Nacional de Engenharia Biomédica, Universidade do Porto, Rua Alfredo Allen 208, 4200-393 Porto, Portugal; ICBAS - Instituto Ciências Biomédicas Abel Salazar, Universidade do Porto, 4150-180 Porto, Portugal; CESPU - Instituto de Investigação e Formação Avançada em Ciências e Tecnologias da Saúde, Rua Central de Gandra 1317, 4585-116 Gandra, Portugal; INL - International Iberian Nanotechnology Laboratory, Avenida Mestre José Veiga, 4715-330 Braga, Portugal., Costa-Pereira AI; CFisUC - Department of Physics, University of Coimbra, Rua Larga, 3004-516 Coimbra, Portugal., Cruz A; INL - International Iberian Nanotechnology Laboratory, Avenida Mestre José Veiga, 4715-330 Braga, Portugal., Ferreira FJ; i3S - Instituto de Investigação e Inovação em Saúde, Universidade do Porto, Rua Alfredo Allen 208, 4200-393 Porto, Portugal; IBMC - Instituto de Biologia Molecular e Celular, Universidade do Porto, Rua Alfredo Allen 208, 4200-393 Porto, Portugal., Gouveia M; CFisUC - Department of Physics, University of Coimbra, Rua Larga, 3004-516 Coimbra, Portugal., Bessa J; i3S - Instituto de Investigação e Inovação em Saúde, Universidade do Porto, Rua Alfredo Allen 208, 4200-393 Porto, Portugal; IBMC - Instituto de Biologia Molecular e Celular, Universidade do Porto, Rua Alfredo Allen 208, 4200-393 Porto, Portugal., Sarmento B; i3S - Instituto de Investigação e Inovação em Saúde, Universidade do Porto, Rua Alfredo Allen 208, 4200-393 Porto, Portugal; INEB - Instituto Nacional de Engenharia Biomédica, Universidade do Porto, Rua Alfredo Allen 208, 4200-393 Porto, Portugal; CESPU - Instituto de Investigação e Formação Avançada em Ciências e Tecnologias da Saúde, Rua Central de Gandra 1317, 4585-116 Gandra, Portugal., Travasso RDM; CFisUC - Department of Physics, University of Coimbra, Rua Larga, 3004-516 Coimbra, Portugal., Mendes Pinto I; i3S - Instituto de Investigação e Inovação em Saúde, Universidade do Porto, Rua Alfredo Allen 208, 4200-393 Porto, Portugal; INL - International Iberian Nanotechnology Laboratory, Avenida Mestre José Veiga, 4715-330 Braga, Portugal. Electronic address: ines.m.pinto@inl.int.
المصدر: Journal of controlled release : official journal of the Controlled Release Society [J Control Release] 2021 Nov 10; Vol. 339, pp. 381-390. Date of Electronic Publication: 2021 Sep 28.
نوع المنشور: Journal Article; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: Elsevier Science Publishers Country of Publication: Netherlands NLM ID: 8607908 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1873-4995 (Electronic) Linking ISSN: 01683659 NLM ISO Abbreviation: J Control Release Subsets: MEDLINE
أسماء مطبوعة: Original Publication: Amsterdam : Elsevier Science Publishers, 1984-
مواضيع طبية MeSH: Brain Neoplasms*/drug therapy , Glioblastoma*/drug therapy, Angiogenesis Inhibitors/therapeutic use ; Bevacizumab/therapeutic use ; Humans ; Neovascularization, Pathologic/drug therapy ; Vascular Endothelial Growth Factor A/therapeutic use
مستخلص: Glioblastoma multiforme (GBM) is the most aggressive and invasive malignant brain cancer. GBM is characterized by a dramatic metabolic imbalance leading to increased secretion of the pro-angiogenic factor VEGF and subsequent abnormal tumor vascularization. In 2009, FDA approved the intravenous administration of bevacizumab, an anti-VEGF monoclonal antibody, as a therapeutic agent for patients with GBM. However, the number of systemic side effects and reduced accessibility of bevacizumab to the central nervous system and consequently to the GBM tumor mass limited its effectiveness in improving patient survival. In this study, we combined experimental and computational modelling to quantitatively characterize the dynamics of VEGF secretion and turnover in GBM and in normal brain cells and simultaneous monitoring of vessel growth. We showed that sequestration of VEGF inside GBM cells, can be used as a novel target for improved bevacizumab-based therapy. We have engineered the VEGF nanotrapper, a cargo system that allows cellular uptake of bevacizumab and inhibits VEGF secretion required for angiogenesis activation and development. Here, we show the therapeutic efficacy of this nanocargo in reducing vascularization and tumor cell mass of GBM in vitro and in vivo cancer models.
(Copyright © 2021 Elsevier B.V. All rights reserved.)
فهرسة مساهمة: Keywords: Computational modelling; Glioblastoma; Intracellular trapping; Nanocargo; VEGF secretion; Vascularization
المشرفين على المادة: 0 (Angiogenesis Inhibitors)
0 (Vascular Endothelial Growth Factor A)
2S9ZZM9Q9V (Bevacizumab)
تواريخ الأحداث: Date Created: 20210930 Date Completed: 20211208 Latest Revision: 20211214
رمز التحديث: 20221213
DOI: 10.1016/j.jconrel.2021.09.031
PMID: 34592385
قاعدة البيانات: MEDLINE
الوصف
تدمد:1873-4995
DOI:10.1016/j.jconrel.2021.09.031