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Recombinant humanised anti-HER2/neu antibody (Herceptin®) induces cellular death of glioblastomas

Glioblastoma multiforme (GBM) remains the most devastating primary tumour in neuro-oncology. Targeting of the human epithelial receptor type 2 (HER2)-neu receptor by specific antibodies is a recent well-established therapy for breast tumours. Human epithelial receptor type 2/neu is a transmembrane t...

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Autores principales: Mineo, J-F, Bordron, A, Quintin-Roué, I, Loisel, S, Ster, K L, Buhé, V, Lagarde, N, Berthou, C
Formato: Texto
Lenguaje:English
Publicado: Nature Publishing Group 2004
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2747695/
https://www.ncbi.nlm.nih.gov/pubmed/15328518
http://dx.doi.org/10.1038/sj.bjc.6602089
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author Mineo, J-F
Bordron, A
Quintin-Roué, I
Loisel, S
Ster, K L
Buhé, V
Lagarde, N
Berthou, C
author_facet Mineo, J-F
Bordron, A
Quintin-Roué, I
Loisel, S
Ster, K L
Buhé, V
Lagarde, N
Berthou, C
author_sort Mineo, J-F
collection PubMed
description Glioblastoma multiforme (GBM) remains the most devastating primary tumour in neuro-oncology. Targeting of the human epithelial receptor type 2 (HER2)-neu receptor by specific antibodies is a recent well-established therapy for breast tumours. Human epithelial receptor type 2/neu is a transmembrane tyrosine/kinase receptor that appears to be important for the regulation of cancer growth. Human epithelial receptor type 2/neu is not expressed in the adult central nervous system, but its expression increases with the degree of astrocytoma anaplasia. The specificity of HER2/neu for tumoral astrocytomas leads us to study in vitro treatment of GBM with anti-HER2/neu antibody. We used human GBM cell lines expressing HER2/neu (A172 express HER2/neu more than U251MG) or not (U87MG) and monoclonal humanised antibody against HER2/neu (Herceptin®). Human epithelial receptor type 2/neu expression was measured by immunohistochemistry and flow cytometry. Direct antibody effect, complement-dependent cytotoxicity and antibody-dependent cellular cytotoxicity were evaluated by different cytometric assays. We have shown, for the first time, the ability of anti-HER2/neu antibodies to induce apoptosis and cellular-dependent cytotoxicity of HER2/neu-expressing GBM cell lines. The results decreased from A172 to U251 and were negative for U87MG, in accordance with the decreasing density of HER2/neu receptors.
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spelling pubmed-27476952009-09-21 Recombinant humanised anti-HER2/neu antibody (Herceptin®) induces cellular death of glioblastomas Mineo, J-F Bordron, A Quintin-Roué, I Loisel, S Ster, K L Buhé, V Lagarde, N Berthou, C Br J Cancer Experimental Therapeutics Glioblastoma multiforme (GBM) remains the most devastating primary tumour in neuro-oncology. Targeting of the human epithelial receptor type 2 (HER2)-neu receptor by specific antibodies is a recent well-established therapy for breast tumours. Human epithelial receptor type 2/neu is a transmembrane tyrosine/kinase receptor that appears to be important for the regulation of cancer growth. Human epithelial receptor type 2/neu is not expressed in the adult central nervous system, but its expression increases with the degree of astrocytoma anaplasia. The specificity of HER2/neu for tumoral astrocytomas leads us to study in vitro treatment of GBM with anti-HER2/neu antibody. We used human GBM cell lines expressing HER2/neu (A172 express HER2/neu more than U251MG) or not (U87MG) and monoclonal humanised antibody against HER2/neu (Herceptin®). Human epithelial receptor type 2/neu expression was measured by immunohistochemistry and flow cytometry. Direct antibody effect, complement-dependent cytotoxicity and antibody-dependent cellular cytotoxicity were evaluated by different cytometric assays. We have shown, for the first time, the ability of anti-HER2/neu antibodies to induce apoptosis and cellular-dependent cytotoxicity of HER2/neu-expressing GBM cell lines. The results decreased from A172 to U251 and were negative for U87MG, in accordance with the decreasing density of HER2/neu receptors. Nature Publishing Group 2004-09-13 2004-08-24 /pmc/articles/PMC2747695/ /pubmed/15328518 http://dx.doi.org/10.1038/sj.bjc.6602089 Text en Copyright © 2004 Cancer Research UK https://creativecommons.org/licenses/by/4.0/This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material.If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit https://creativecommons.org/licenses/by/4.0/.
spellingShingle Experimental Therapeutics
Mineo, J-F
Bordron, A
Quintin-Roué, I
Loisel, S
Ster, K L
Buhé, V
Lagarde, N
Berthou, C
Recombinant humanised anti-HER2/neu antibody (Herceptin®) induces cellular death of glioblastomas
title Recombinant humanised anti-HER2/neu antibody (Herceptin®) induces cellular death of glioblastomas
title_full Recombinant humanised anti-HER2/neu antibody (Herceptin®) induces cellular death of glioblastomas
title_fullStr Recombinant humanised anti-HER2/neu antibody (Herceptin®) induces cellular death of glioblastomas
title_full_unstemmed Recombinant humanised anti-HER2/neu antibody (Herceptin®) induces cellular death of glioblastomas
title_short Recombinant humanised anti-HER2/neu antibody (Herceptin®) induces cellular death of glioblastomas
title_sort recombinant humanised anti-her2/neu antibody (herceptin®) induces cellular death of glioblastomas
topic Experimental Therapeutics
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2747695/
https://www.ncbi.nlm.nih.gov/pubmed/15328518
http://dx.doi.org/10.1038/sj.bjc.6602089
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