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Glioma cells showing IDH1 mutation cannot be propagated in standard cell culture conditions

BACKGROUND: It has recently been reported by several sources that original (i.e., present in vivo) glioma cell phenotypes or genotypes cannot be maintained in vitro. For example, glioblastoma cell lines presenting EGFR amplification cannot be established. METHODS AND RESULTS: IDH1 sequencing and los...

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Autores principales: Piaskowski, S, Bienkowski, M, Stoczynska-Fidelus, E, Stawski, R, Sieruta, M, Szybka, M, Papierz, W, Wolanczyk, M, Jaskolski, D J, Liberski, P P, Rieske, P
Formato: Texto
Lenguaje:English
Publicado: Nature Publishing Group 2011
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3065269/
https://www.ncbi.nlm.nih.gov/pubmed/21326241
http://dx.doi.org/10.1038/bjc.2011.27
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author Piaskowski, S
Bienkowski, M
Stoczynska-Fidelus, E
Stawski, R
Sieruta, M
Szybka, M
Papierz, W
Wolanczyk, M
Jaskolski, D J
Liberski, P P
Rieske, P
author_facet Piaskowski, S
Bienkowski, M
Stoczynska-Fidelus, E
Stawski, R
Sieruta, M
Szybka, M
Papierz, W
Wolanczyk, M
Jaskolski, D J
Liberski, P P
Rieske, P
author_sort Piaskowski, S
collection PubMed
description BACKGROUND: It has recently been reported by several sources that original (i.e., present in vivo) glioma cell phenotypes or genotypes cannot be maintained in vitro. For example, glioblastoma cell lines presenting EGFR amplification cannot be established. METHODS AND RESULTS: IDH1 sequencing and loss of heterozygosity analysis was performed for 15 surgery samples of astrocytoma and early and late passages of cells derived from those and for 11 archival samples. We were not able to culture tumour cells presenting IDH1 mutations originating from currently proceeded 10 tumours; the same results were observed in 7 samples of archival material. CONCLUSION: The IDH1 mutation is expected to be almost mutually exclusive with EGFR amplification, so glioma cells with IDH1 mutations seem to represent a new group of tumour cells, which cannot be readily analysed in vitro because of their elimination. The reasons for this intriguing phenomenon should be investigated since its understanding can help to define a new therapeutic approach based on simulating in vivo conditions, responsible for tumour cells elimination in vitro. Moreover, a new model for culturing glioma cells in vitro should be designed since the current one does not provide conditions corresponding to in vivo growth.
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spelling pubmed-30652692012-03-15 Glioma cells showing IDH1 mutation cannot be propagated in standard cell culture conditions Piaskowski, S Bienkowski, M Stoczynska-Fidelus, E Stawski, R Sieruta, M Szybka, M Papierz, W Wolanczyk, M Jaskolski, D J Liberski, P P Rieske, P Br J Cancer Short Communication BACKGROUND: It has recently been reported by several sources that original (i.e., present in vivo) glioma cell phenotypes or genotypes cannot be maintained in vitro. For example, glioblastoma cell lines presenting EGFR amplification cannot be established. METHODS AND RESULTS: IDH1 sequencing and loss of heterozygosity analysis was performed for 15 surgery samples of astrocytoma and early and late passages of cells derived from those and for 11 archival samples. We were not able to culture tumour cells presenting IDH1 mutations originating from currently proceeded 10 tumours; the same results were observed in 7 samples of archival material. CONCLUSION: The IDH1 mutation is expected to be almost mutually exclusive with EGFR amplification, so glioma cells with IDH1 mutations seem to represent a new group of tumour cells, which cannot be readily analysed in vitro because of their elimination. The reasons for this intriguing phenomenon should be investigated since its understanding can help to define a new therapeutic approach based on simulating in vivo conditions, responsible for tumour cells elimination in vitro. Moreover, a new model for culturing glioma cells in vitro should be designed since the current one does not provide conditions corresponding to in vivo growth. Nature Publishing Group 2011-03-15 2011-02-15 /pmc/articles/PMC3065269/ /pubmed/21326241 http://dx.doi.org/10.1038/bjc.2011.27 Text en Copyright © 2011 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 Short Communication
Piaskowski, S
Bienkowski, M
Stoczynska-Fidelus, E
Stawski, R
Sieruta, M
Szybka, M
Papierz, W
Wolanczyk, M
Jaskolski, D J
Liberski, P P
Rieske, P
Glioma cells showing IDH1 mutation cannot be propagated in standard cell culture conditions
title Glioma cells showing IDH1 mutation cannot be propagated in standard cell culture conditions
title_full Glioma cells showing IDH1 mutation cannot be propagated in standard cell culture conditions
title_fullStr Glioma cells showing IDH1 mutation cannot be propagated in standard cell culture conditions
title_full_unstemmed Glioma cells showing IDH1 mutation cannot be propagated in standard cell culture conditions
title_short Glioma cells showing IDH1 mutation cannot be propagated in standard cell culture conditions
title_sort glioma cells showing idh1 mutation cannot be propagated in standard cell culture conditions
topic Short Communication
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3065269/
https://www.ncbi.nlm.nih.gov/pubmed/21326241
http://dx.doi.org/10.1038/bjc.2011.27
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