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CBMT-21. TERT PROMOTER-MUTANT GLIOBLASTOMAS EXHIBIT DEPENDENCY ON TELOMERASE
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Zeitschriftentitel: | Neuro-Oncology |
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Personen und Körperschaften: | , , , |
In: | Neuro-Oncology, 21, 2019, Supplement_6, S. vi37-vi37 |
Format: | E-Article |
Sprache: | Englisch |
veröffentlicht: |
Oxford University Press (OUP)
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Schlagwörter: |
author_facet |
Aquilanti, Elisa Baird, Duncan Watson, Jacqueline Meyerson, Matthew Aquilanti, Elisa Baird, Duncan Watson, Jacqueline Meyerson, Matthew |
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author |
Aquilanti, Elisa Baird, Duncan Watson, Jacqueline Meyerson, Matthew |
spellingShingle |
Aquilanti, Elisa Baird, Duncan Watson, Jacqueline Meyerson, Matthew Neuro-Oncology CBMT-21. TERT PROMOTER-MUTANT GLIOBLASTOMAS EXHIBIT DEPENDENCY ON TELOMERASE Cancer Research Neurology (clinical) Oncology |
author_sort |
aquilanti, elisa |
spelling |
Aquilanti, Elisa Baird, Duncan Watson, Jacqueline Meyerson, Matthew 1522-8517 1523-5866 Oxford University Press (OUP) Cancer Research Neurology (clinical) Oncology http://dx.doi.org/10.1093/neuonc/noz175.143 <jats:title>Abstract</jats:title> <jats:p>TERT promoter mutations are among the most common somatic alterations in cancer and they occur in about 80% of IDH-wildtype glioblastomas. TERT promoter mutations were found to reactivate telomerase by providing a novel binding site for the GABP transcription factor. While the effects of telomerase ablation are well understood in mice and somatic human cells, these effects in cancer are yet to be fully elucidated. In this study, we used a genetic approach with CRISPR-interference to knock down telomerase in TERT promoter-mutant glioblastoma cell lines. We show that this leads to a gradual and significant reduction in proliferation. This phenotype ultimately culminates in telomere crisis, with telomere shortening, activation of the DNA damage response pathway and formation of chromatin bridges. These data suggest that anti-telomerase therapy is a potential effective approach for glioblastoma tumors.</jats:p> CBMT-21. TERT PROMOTER-MUTANT GLIOBLASTOMAS EXHIBIT DEPENDENCY ON TELOMERASE Neuro-Oncology |
doi_str_mv |
10.1093/neuonc/noz175.143 |
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Oxford University Press (OUP) |
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Neuro-Oncology |
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title |
CBMT-21. TERT PROMOTER-MUTANT GLIOBLASTOMAS EXHIBIT DEPENDENCY ON TELOMERASE |
title_unstemmed |
CBMT-21. TERT PROMOTER-MUTANT GLIOBLASTOMAS EXHIBIT DEPENDENCY ON TELOMERASE |
title_full |
CBMT-21. TERT PROMOTER-MUTANT GLIOBLASTOMAS EXHIBIT DEPENDENCY ON TELOMERASE |
title_fullStr |
CBMT-21. TERT PROMOTER-MUTANT GLIOBLASTOMAS EXHIBIT DEPENDENCY ON TELOMERASE |
title_full_unstemmed |
CBMT-21. TERT PROMOTER-MUTANT GLIOBLASTOMAS EXHIBIT DEPENDENCY ON TELOMERASE |
title_short |
CBMT-21. TERT PROMOTER-MUTANT GLIOBLASTOMAS EXHIBIT DEPENDENCY ON TELOMERASE |
title_sort |
cbmt-21. tert promoter-mutant glioblastomas exhibit dependency on telomerase |
topic |
Cancer Research Neurology (clinical) Oncology |
url |
http://dx.doi.org/10.1093/neuonc/noz175.143 |
publishDate |
2019 |
physical |
vi37-vi37 |
description |
<jats:title>Abstract</jats:title>
<jats:p>TERT promoter mutations are among the most common somatic alterations in cancer and they occur in about 80% of IDH-wildtype glioblastomas. TERT promoter mutations were found to reactivate telomerase by providing a novel binding site for the GABP transcription factor. While the effects of telomerase ablation are well understood in mice and somatic human cells, these effects in cancer are yet to be fully elucidated. In this study, we used a genetic approach with CRISPR-interference to knock down telomerase in TERT promoter-mutant glioblastoma cell lines. We show that this leads to a gradual and significant reduction in proliferation. This phenotype ultimately culminates in telomere crisis, with telomere shortening, activation of the DNA damage response pathway and formation of chromatin bridges. These data suggest that anti-telomerase therapy is a potential effective approach for glioblastoma tumors.</jats:p> |
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author | Aquilanti, Elisa, Baird, Duncan, Watson, Jacqueline, Meyerson, Matthew |
author_facet | Aquilanti, Elisa, Baird, Duncan, Watson, Jacqueline, Meyerson, Matthew, Aquilanti, Elisa, Baird, Duncan, Watson, Jacqueline, Meyerson, Matthew |
author_sort | aquilanti, elisa |
container_issue | Supplement_6 |
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description | <jats:title>Abstract</jats:title> <jats:p>TERT promoter mutations are among the most common somatic alterations in cancer and they occur in about 80% of IDH-wildtype glioblastomas. TERT promoter mutations were found to reactivate telomerase by providing a novel binding site for the GABP transcription factor. While the effects of telomerase ablation are well understood in mice and somatic human cells, these effects in cancer are yet to be fully elucidated. In this study, we used a genetic approach with CRISPR-interference to knock down telomerase in TERT promoter-mutant glioblastoma cell lines. We show that this leads to a gradual and significant reduction in proliferation. This phenotype ultimately culminates in telomere crisis, with telomere shortening, activation of the DNA damage response pathway and formation of chromatin bridges. These data suggest that anti-telomerase therapy is a potential effective approach for glioblastoma tumors.</jats:p> |
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spelling | Aquilanti, Elisa Baird, Duncan Watson, Jacqueline Meyerson, Matthew 1522-8517 1523-5866 Oxford University Press (OUP) Cancer Research Neurology (clinical) Oncology http://dx.doi.org/10.1093/neuonc/noz175.143 <jats:title>Abstract</jats:title> <jats:p>TERT promoter mutations are among the most common somatic alterations in cancer and they occur in about 80% of IDH-wildtype glioblastomas. TERT promoter mutations were found to reactivate telomerase by providing a novel binding site for the GABP transcription factor. While the effects of telomerase ablation are well understood in mice and somatic human cells, these effects in cancer are yet to be fully elucidated. In this study, we used a genetic approach with CRISPR-interference to knock down telomerase in TERT promoter-mutant glioblastoma cell lines. We show that this leads to a gradual and significant reduction in proliferation. This phenotype ultimately culminates in telomere crisis, with telomere shortening, activation of the DNA damage response pathway and formation of chromatin bridges. These data suggest that anti-telomerase therapy is a potential effective approach for glioblastoma tumors.</jats:p> CBMT-21. TERT PROMOTER-MUTANT GLIOBLASTOMAS EXHIBIT DEPENDENCY ON TELOMERASE Neuro-Oncology |
spellingShingle | Aquilanti, Elisa, Baird, Duncan, Watson, Jacqueline, Meyerson, Matthew, Neuro-Oncology, CBMT-21. TERT PROMOTER-MUTANT GLIOBLASTOMAS EXHIBIT DEPENDENCY ON TELOMERASE, Cancer Research, Neurology (clinical), Oncology |
title | CBMT-21. TERT PROMOTER-MUTANT GLIOBLASTOMAS EXHIBIT DEPENDENCY ON TELOMERASE |
title_full | CBMT-21. TERT PROMOTER-MUTANT GLIOBLASTOMAS EXHIBIT DEPENDENCY ON TELOMERASE |
title_fullStr | CBMT-21. TERT PROMOTER-MUTANT GLIOBLASTOMAS EXHIBIT DEPENDENCY ON TELOMERASE |
title_full_unstemmed | CBMT-21. TERT PROMOTER-MUTANT GLIOBLASTOMAS EXHIBIT DEPENDENCY ON TELOMERASE |
title_short | CBMT-21. TERT PROMOTER-MUTANT GLIOBLASTOMAS EXHIBIT DEPENDENCY ON TELOMERASE |
title_sort | cbmt-21. tert promoter-mutant glioblastomas exhibit dependency on telomerase |
title_unstemmed | CBMT-21. TERT PROMOTER-MUTANT GLIOBLASTOMAS EXHIBIT DEPENDENCY ON TELOMERASE |
topic | Cancer Research, Neurology (clinical), Oncology |
url | http://dx.doi.org/10.1093/neuonc/noz175.143 |