Alternative lengthening of telomeres is the major telomere maintenance mechanism in astrocytoma with isocitrate dehydrogenase 1 mutation
Purpose Isocitrate dehydrogenase 1 (IDH1) mutations are associated with improved survival in gliomas. Depending on the IDH1 status, TERT promoter mutations affect prognosis. IDH1 mutations are associated with alpha-thalassemia/mental retardation syndrome X-linked (ATRX) mutations and alternative len...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Ferreira, Monica Sofia Ventura [verfasserIn] Sørensen, Mia Dahl [verfasserIn] Pusch, Stefan [verfasserIn] Beier, Dagmar [verfasserIn] Bouillon, Anne-Sophie [verfasserIn] Kristensen, Bjarne Winther [verfasserIn] Brümmendorf, Tim Henrik [verfasserIn] Beier, Christoph Patrick [verfasserIn] Beier, Fabian [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2020 |
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| Schlagwörter: |
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| Übergeordnetes Werk: |
Enthalten in: Journal of neuro-oncology - Dordrecht [u.a.] : Springer Science + Business Media B.V, 1983, 147(2020), 1 vom: 20. Jan., Seite 1-14 |
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| Übergeordnetes Werk: |
volume:147 ; year:2020 ; number:1 ; day:20 ; month:01 ; pages:1-14 |
| Links: |
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| DOI / URN: |
10.1007/s11060-020-03394-y |
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| Katalog-ID: |
SPR039118487 |
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| 100 | 1 | |a Ferreira, Monica Sofia Ventura |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Alternative lengthening of telomeres is the major telomere maintenance mechanism in astrocytoma with isocitrate dehydrogenase 1 mutation |
| 264 | 1 | |c 2020 | |
| 336 | |a Text |b txt |2 rdacontent | ||
| 337 | |a Computermedien |b c |2 rdamedia | ||
| 338 | |a Online-Ressource |b cr |2 rdacarrier | ||
| 520 | |a Purpose Isocitrate dehydrogenase 1 (IDH1) mutations are associated with improved survival in gliomas. Depending on the IDH1 status, TERT promoter mutations affect prognosis. IDH1 mutations are associated with alpha-thalassemia/mental retardation syndrome X-linked (ATRX) mutations and alternative lengthening of telomeres (ALT), suggesting an interaction between IDH1 and telomeres. However, little is known how IDH1 mutations affect telomere maintenance. Methods We analyzed cell-specific telomere length (CS-TL) on a single cell level in 46 astrocytoma samples (WHO II-IV) by modified immune-quantitative fluorescence in situ hybridization, using endothelial cells as internal reference. In the same samples, we determined IDH1/TERT promoter mutation status and ATRX expression. The interaction of $ IDH1^{R132H} $ mutation and CS-TL was studied in vitro using an $ IDH1^{R132H} $ doxycycline-inducible glioma cell line system. Results Virtually all $ ALT^{positive} $ astrocytomas had normal TERT promoter and lacked ATRX expression. Further, all $ ALT^{positive} $ samples had $ IDH1^{R132H} $ mutations, resulting in a significantly longer CS-TL of $ IDH1^{R132H} $ gliomas, when compared to their wildtype counterparts. Conversely, TERT promotor mutations were associated with $ IDH^{wildtype} $, ATRX expression, lack of ALT and short CS-TL. ALT, TERT promoter mutations, and CS-TL remained without prognostic significance, when correcting for IDH1 status. In vitro, overexpression of $ IDH^{R132H} $ in the glioma cell line LN319 resulted in downregulation of ATRX and rapid TERT-independent telomere lengthening consistent with ALT. Conclusion ALT is the major telomere maintenance mechanism in $ IDH^{R132H} $ mutated astrocytomas, while TERT promoter mutations were associated with $ IDH^{wildtype} $ glioma. $ IDH1^{R132H} $ downregulates ATRX expression in vitro resulting in ALT, which may contribute to the strong association of $ IDH1^{R132H} $ mutations, ATRX loss, and ALT. | ||
| 650 | 4 | |a Isocitrate dehydrogenase |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a D2HG |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Telomerase |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Telomere length |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Q-FISH |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a TERT promoter |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a ALT |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a ATRX |7 (dpeaa)DE-He213 | |
| 700 | 1 | |a Sørensen, Mia Dahl |e verfasserin |4 aut | |
| 700 | 1 | |a Pusch, Stefan |e verfasserin |4 aut | |
| 700 | 1 | |a Beier, Dagmar |e verfasserin |4 aut | |
| 700 | 1 | |a Bouillon, Anne-Sophie |e verfasserin |4 aut | |
| 700 | 1 | |a Kristensen, Bjarne Winther |e verfasserin |4 aut | |
| 700 | 1 | |a Brümmendorf, Tim Henrik |e verfasserin |4 aut | |
| 700 | 1 | |a Beier, Christoph Patrick |e verfasserin |4 aut | |
| 700 | 1 | |a Beier, Fabian |e verfasserin |4 aut | |
| 773 | 0 | 8 | |i Enthalten in |t Journal of neuro-oncology |d Dordrecht [u.a.] : Springer Science + Business Media B.V, 1983 |g 147(2020), 1 vom: 20. Jan., Seite 1-14 |w (DE-627)32046122X |w (DE-600)2007293-4 |x 1573-7373 |7 nnns |
| 773 | 1 | 8 | |g volume:147 |g year:2020 |g number:1 |g day:20 |g month:01 |g pages:1-14 |
| 856 | 4 | 0 | |u https://dx.doi.org/10.1007/s11060-020-03394-y |z kostenfrei |3 Volltext |
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10.1007/s11060-020-03394-y doi (DE-627)SPR039118487 (SPR)s11060-020-03394-y-e DE-627 ger DE-627 rakwb eng 610 ASE 44.81 bkl 44.90 bkl Ferreira, Monica Sofia Ventura verfasserin aut Alternative lengthening of telomeres is the major telomere maintenance mechanism in astrocytoma with isocitrate dehydrogenase 1 mutation 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Purpose Isocitrate dehydrogenase 1 (IDH1) mutations are associated with improved survival in gliomas. Depending on the IDH1 status, TERT promoter mutations affect prognosis. IDH1 mutations are associated with alpha-thalassemia/mental retardation syndrome X-linked (ATRX) mutations and alternative lengthening of telomeres (ALT), suggesting an interaction between IDH1 and telomeres. However, little is known how IDH1 mutations affect telomere maintenance. Methods We analyzed cell-specific telomere length (CS-TL) on a single cell level in 46 astrocytoma samples (WHO II-IV) by modified immune-quantitative fluorescence in situ hybridization, using endothelial cells as internal reference. In the same samples, we determined IDH1/TERT promoter mutation status and ATRX expression. The interaction of $ IDH1^{R132H} $ mutation and CS-TL was studied in vitro using an $ IDH1^{R132H} $ doxycycline-inducible glioma cell line system. Results Virtually all $ ALT^{positive} $ astrocytomas had normal TERT promoter and lacked ATRX expression. Further, all $ ALT^{positive} $ samples had $ IDH1^{R132H} $ mutations, resulting in a significantly longer CS-TL of $ IDH1^{R132H} $ gliomas, when compared to their wildtype counterparts. Conversely, TERT promotor mutations were associated with $ IDH^{wildtype} $, ATRX expression, lack of ALT and short CS-TL. ALT, TERT promoter mutations, and CS-TL remained without prognostic significance, when correcting for IDH1 status. In vitro, overexpression of $ IDH^{R132H} $ in the glioma cell line LN319 resulted in downregulation of ATRX and rapid TERT-independent telomere lengthening consistent with ALT. Conclusion ALT is the major telomere maintenance mechanism in $ IDH^{R132H} $ mutated astrocytomas, while TERT promoter mutations were associated with $ IDH^{wildtype} $ glioma. $ IDH1^{R132H} $ downregulates ATRX expression in vitro resulting in ALT, which may contribute to the strong association of $ IDH1^{R132H} $ mutations, ATRX loss, and ALT. Isocitrate dehydrogenase (dpeaa)DE-He213 D2HG (dpeaa)DE-He213 Telomerase (dpeaa)DE-He213 Telomere length (dpeaa)DE-He213 Q-FISH (dpeaa)DE-He213 TERT promoter (dpeaa)DE-He213 ALT (dpeaa)DE-He213 ATRX (dpeaa)DE-He213 Sørensen, Mia Dahl verfasserin aut Pusch, Stefan verfasserin aut Beier, Dagmar verfasserin aut Bouillon, Anne-Sophie verfasserin aut Kristensen, Bjarne Winther verfasserin aut Brümmendorf, Tim Henrik verfasserin aut Beier, Christoph Patrick verfasserin aut Beier, Fabian verfasserin aut Enthalten in Journal of neuro-oncology Dordrecht [u.a.] : Springer Science + Business Media B.V, 1983 147(2020), 1 vom: 20. Jan., Seite 1-14 (DE-627)32046122X (DE-600)2007293-4 1573-7373 nnns volume:147 year:2020 number:1 day:20 month:01 pages:1-14 https://dx.doi.org/10.1007/s11060-020-03394-y kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.81 ASE 44.90 ASE AR 147 2020 1 20 01 1-14 |
| spelling |
10.1007/s11060-020-03394-y doi (DE-627)SPR039118487 (SPR)s11060-020-03394-y-e DE-627 ger DE-627 rakwb eng 610 ASE 44.81 bkl 44.90 bkl Ferreira, Monica Sofia Ventura verfasserin aut Alternative lengthening of telomeres is the major telomere maintenance mechanism in astrocytoma with isocitrate dehydrogenase 1 mutation 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Purpose Isocitrate dehydrogenase 1 (IDH1) mutations are associated with improved survival in gliomas. Depending on the IDH1 status, TERT promoter mutations affect prognosis. IDH1 mutations are associated with alpha-thalassemia/mental retardation syndrome X-linked (ATRX) mutations and alternative lengthening of telomeres (ALT), suggesting an interaction between IDH1 and telomeres. However, little is known how IDH1 mutations affect telomere maintenance. Methods We analyzed cell-specific telomere length (CS-TL) on a single cell level in 46 astrocytoma samples (WHO II-IV) by modified immune-quantitative fluorescence in situ hybridization, using endothelial cells as internal reference. In the same samples, we determined IDH1/TERT promoter mutation status and ATRX expression. The interaction of $ IDH1^{R132H} $ mutation and CS-TL was studied in vitro using an $ IDH1^{R132H} $ doxycycline-inducible glioma cell line system. Results Virtually all $ ALT^{positive} $ astrocytomas had normal TERT promoter and lacked ATRX expression. Further, all $ ALT^{positive} $ samples had $ IDH1^{R132H} $ mutations, resulting in a significantly longer CS-TL of $ IDH1^{R132H} $ gliomas, when compared to their wildtype counterparts. Conversely, TERT promotor mutations were associated with $ IDH^{wildtype} $, ATRX expression, lack of ALT and short CS-TL. ALT, TERT promoter mutations, and CS-TL remained without prognostic significance, when correcting for IDH1 status. In vitro, overexpression of $ IDH^{R132H} $ in the glioma cell line LN319 resulted in downregulation of ATRX and rapid TERT-independent telomere lengthening consistent with ALT. Conclusion ALT is the major telomere maintenance mechanism in $ IDH^{R132H} $ mutated astrocytomas, while TERT promoter mutations were associated with $ IDH^{wildtype} $ glioma. $ IDH1^{R132H} $ downregulates ATRX expression in vitro resulting in ALT, which may contribute to the strong association of $ IDH1^{R132H} $ mutations, ATRX loss, and ALT. Isocitrate dehydrogenase (dpeaa)DE-He213 D2HG (dpeaa)DE-He213 Telomerase (dpeaa)DE-He213 Telomere length (dpeaa)DE-He213 Q-FISH (dpeaa)DE-He213 TERT promoter (dpeaa)DE-He213 ALT (dpeaa)DE-He213 ATRX (dpeaa)DE-He213 Sørensen, Mia Dahl verfasserin aut Pusch, Stefan verfasserin aut Beier, Dagmar verfasserin aut Bouillon, Anne-Sophie verfasserin aut Kristensen, Bjarne Winther verfasserin aut Brümmendorf, Tim Henrik verfasserin aut Beier, Christoph Patrick verfasserin aut Beier, Fabian verfasserin aut Enthalten in Journal of neuro-oncology Dordrecht [u.a.] : Springer Science + Business Media B.V, 1983 147(2020), 1 vom: 20. Jan., Seite 1-14 (DE-627)32046122X (DE-600)2007293-4 1573-7373 nnns volume:147 year:2020 number:1 day:20 month:01 pages:1-14 https://dx.doi.org/10.1007/s11060-020-03394-y kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.81 ASE 44.90 ASE AR 147 2020 1 20 01 1-14 |
| allfields_unstemmed |
10.1007/s11060-020-03394-y doi (DE-627)SPR039118487 (SPR)s11060-020-03394-y-e DE-627 ger DE-627 rakwb eng 610 ASE 44.81 bkl 44.90 bkl Ferreira, Monica Sofia Ventura verfasserin aut Alternative lengthening of telomeres is the major telomere maintenance mechanism in astrocytoma with isocitrate dehydrogenase 1 mutation 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Purpose Isocitrate dehydrogenase 1 (IDH1) mutations are associated with improved survival in gliomas. Depending on the IDH1 status, TERT promoter mutations affect prognosis. IDH1 mutations are associated with alpha-thalassemia/mental retardation syndrome X-linked (ATRX) mutations and alternative lengthening of telomeres (ALT), suggesting an interaction between IDH1 and telomeres. However, little is known how IDH1 mutations affect telomere maintenance. Methods We analyzed cell-specific telomere length (CS-TL) on a single cell level in 46 astrocytoma samples (WHO II-IV) by modified immune-quantitative fluorescence in situ hybridization, using endothelial cells as internal reference. In the same samples, we determined IDH1/TERT promoter mutation status and ATRX expression. The interaction of $ IDH1^{R132H} $ mutation and CS-TL was studied in vitro using an $ IDH1^{R132H} $ doxycycline-inducible glioma cell line system. Results Virtually all $ ALT^{positive} $ astrocytomas had normal TERT promoter and lacked ATRX expression. Further, all $ ALT^{positive} $ samples had $ IDH1^{R132H} $ mutations, resulting in a significantly longer CS-TL of $ IDH1^{R132H} $ gliomas, when compared to their wildtype counterparts. Conversely, TERT promotor mutations were associated with $ IDH^{wildtype} $, ATRX expression, lack of ALT and short CS-TL. ALT, TERT promoter mutations, and CS-TL remained without prognostic significance, when correcting for IDH1 status. In vitro, overexpression of $ IDH^{R132H} $ in the glioma cell line LN319 resulted in downregulation of ATRX and rapid TERT-independent telomere lengthening consistent with ALT. Conclusion ALT is the major telomere maintenance mechanism in $ IDH^{R132H} $ mutated astrocytomas, while TERT promoter mutations were associated with $ IDH^{wildtype} $ glioma. $ IDH1^{R132H} $ downregulates ATRX expression in vitro resulting in ALT, which may contribute to the strong association of $ IDH1^{R132H} $ mutations, ATRX loss, and ALT. Isocitrate dehydrogenase (dpeaa)DE-He213 D2HG (dpeaa)DE-He213 Telomerase (dpeaa)DE-He213 Telomere length (dpeaa)DE-He213 Q-FISH (dpeaa)DE-He213 TERT promoter (dpeaa)DE-He213 ALT (dpeaa)DE-He213 ATRX (dpeaa)DE-He213 Sørensen, Mia Dahl verfasserin aut Pusch, Stefan verfasserin aut Beier, Dagmar verfasserin aut Bouillon, Anne-Sophie verfasserin aut Kristensen, Bjarne Winther verfasserin aut Brümmendorf, Tim Henrik verfasserin aut Beier, Christoph Patrick verfasserin aut Beier, Fabian verfasserin aut Enthalten in Journal of neuro-oncology Dordrecht [u.a.] : Springer Science + Business Media B.V, 1983 147(2020), 1 vom: 20. Jan., Seite 1-14 (DE-627)32046122X (DE-600)2007293-4 1573-7373 nnns volume:147 year:2020 number:1 day:20 month:01 pages:1-14 https://dx.doi.org/10.1007/s11060-020-03394-y kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.81 ASE 44.90 ASE AR 147 2020 1 20 01 1-14 |
| allfieldsGer |
10.1007/s11060-020-03394-y doi (DE-627)SPR039118487 (SPR)s11060-020-03394-y-e DE-627 ger DE-627 rakwb eng 610 ASE 44.81 bkl 44.90 bkl Ferreira, Monica Sofia Ventura verfasserin aut Alternative lengthening of telomeres is the major telomere maintenance mechanism in astrocytoma with isocitrate dehydrogenase 1 mutation 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Purpose Isocitrate dehydrogenase 1 (IDH1) mutations are associated with improved survival in gliomas. Depending on the IDH1 status, TERT promoter mutations affect prognosis. IDH1 mutations are associated with alpha-thalassemia/mental retardation syndrome X-linked (ATRX) mutations and alternative lengthening of telomeres (ALT), suggesting an interaction between IDH1 and telomeres. However, little is known how IDH1 mutations affect telomere maintenance. Methods We analyzed cell-specific telomere length (CS-TL) on a single cell level in 46 astrocytoma samples (WHO II-IV) by modified immune-quantitative fluorescence in situ hybridization, using endothelial cells as internal reference. In the same samples, we determined IDH1/TERT promoter mutation status and ATRX expression. The interaction of $ IDH1^{R132H} $ mutation and CS-TL was studied in vitro using an $ IDH1^{R132H} $ doxycycline-inducible glioma cell line system. Results Virtually all $ ALT^{positive} $ astrocytomas had normal TERT promoter and lacked ATRX expression. Further, all $ ALT^{positive} $ samples had $ IDH1^{R132H} $ mutations, resulting in a significantly longer CS-TL of $ IDH1^{R132H} $ gliomas, when compared to their wildtype counterparts. Conversely, TERT promotor mutations were associated with $ IDH^{wildtype} $, ATRX expression, lack of ALT and short CS-TL. ALT, TERT promoter mutations, and CS-TL remained without prognostic significance, when correcting for IDH1 status. In vitro, overexpression of $ IDH^{R132H} $ in the glioma cell line LN319 resulted in downregulation of ATRX and rapid TERT-independent telomere lengthening consistent with ALT. Conclusion ALT is the major telomere maintenance mechanism in $ IDH^{R132H} $ mutated astrocytomas, while TERT promoter mutations were associated with $ IDH^{wildtype} $ glioma. $ IDH1^{R132H} $ downregulates ATRX expression in vitro resulting in ALT, which may contribute to the strong association of $ IDH1^{R132H} $ mutations, ATRX loss, and ALT. Isocitrate dehydrogenase (dpeaa)DE-He213 D2HG (dpeaa)DE-He213 Telomerase (dpeaa)DE-He213 Telomere length (dpeaa)DE-He213 Q-FISH (dpeaa)DE-He213 TERT promoter (dpeaa)DE-He213 ALT (dpeaa)DE-He213 ATRX (dpeaa)DE-He213 Sørensen, Mia Dahl verfasserin aut Pusch, Stefan verfasserin aut Beier, Dagmar verfasserin aut Bouillon, Anne-Sophie verfasserin aut Kristensen, Bjarne Winther verfasserin aut Brümmendorf, Tim Henrik verfasserin aut Beier, Christoph Patrick verfasserin aut Beier, Fabian verfasserin aut Enthalten in Journal of neuro-oncology Dordrecht [u.a.] : Springer Science + Business Media B.V, 1983 147(2020), 1 vom: 20. Jan., Seite 1-14 (DE-627)32046122X (DE-600)2007293-4 1573-7373 nnns volume:147 year:2020 number:1 day:20 month:01 pages:1-14 https://dx.doi.org/10.1007/s11060-020-03394-y kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.81 ASE 44.90 ASE AR 147 2020 1 20 01 1-14 |
| allfieldsSound |
10.1007/s11060-020-03394-y doi (DE-627)SPR039118487 (SPR)s11060-020-03394-y-e DE-627 ger DE-627 rakwb eng 610 ASE 44.81 bkl 44.90 bkl Ferreira, Monica Sofia Ventura verfasserin aut Alternative lengthening of telomeres is the major telomere maintenance mechanism in astrocytoma with isocitrate dehydrogenase 1 mutation 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Purpose Isocitrate dehydrogenase 1 (IDH1) mutations are associated with improved survival in gliomas. Depending on the IDH1 status, TERT promoter mutations affect prognosis. IDH1 mutations are associated with alpha-thalassemia/mental retardation syndrome X-linked (ATRX) mutations and alternative lengthening of telomeres (ALT), suggesting an interaction between IDH1 and telomeres. However, little is known how IDH1 mutations affect telomere maintenance. Methods We analyzed cell-specific telomere length (CS-TL) on a single cell level in 46 astrocytoma samples (WHO II-IV) by modified immune-quantitative fluorescence in situ hybridization, using endothelial cells as internal reference. In the same samples, we determined IDH1/TERT promoter mutation status and ATRX expression. The interaction of $ IDH1^{R132H} $ mutation and CS-TL was studied in vitro using an $ IDH1^{R132H} $ doxycycline-inducible glioma cell line system. Results Virtually all $ ALT^{positive} $ astrocytomas had normal TERT promoter and lacked ATRX expression. Further, all $ ALT^{positive} $ samples had $ IDH1^{R132H} $ mutations, resulting in a significantly longer CS-TL of $ IDH1^{R132H} $ gliomas, when compared to their wildtype counterparts. Conversely, TERT promotor mutations were associated with $ IDH^{wildtype} $, ATRX expression, lack of ALT and short CS-TL. ALT, TERT promoter mutations, and CS-TL remained without prognostic significance, when correcting for IDH1 status. In vitro, overexpression of $ IDH^{R132H} $ in the glioma cell line LN319 resulted in downregulation of ATRX and rapid TERT-independent telomere lengthening consistent with ALT. Conclusion ALT is the major telomere maintenance mechanism in $ IDH^{R132H} $ mutated astrocytomas, while TERT promoter mutations were associated with $ IDH^{wildtype} $ glioma. $ IDH1^{R132H} $ downregulates ATRX expression in vitro resulting in ALT, which may contribute to the strong association of $ IDH1^{R132H} $ mutations, ATRX loss, and ALT. Isocitrate dehydrogenase (dpeaa)DE-He213 D2HG (dpeaa)DE-He213 Telomerase (dpeaa)DE-He213 Telomere length (dpeaa)DE-He213 Q-FISH (dpeaa)DE-He213 TERT promoter (dpeaa)DE-He213 ALT (dpeaa)DE-He213 ATRX (dpeaa)DE-He213 Sørensen, Mia Dahl verfasserin aut Pusch, Stefan verfasserin aut Beier, Dagmar verfasserin aut Bouillon, Anne-Sophie verfasserin aut Kristensen, Bjarne Winther verfasserin aut Brümmendorf, Tim Henrik verfasserin aut Beier, Christoph Patrick verfasserin aut Beier, Fabian verfasserin aut Enthalten in Journal of neuro-oncology Dordrecht [u.a.] : Springer Science + Business Media B.V, 1983 147(2020), 1 vom: 20. Jan., Seite 1-14 (DE-627)32046122X (DE-600)2007293-4 1573-7373 nnns volume:147 year:2020 number:1 day:20 month:01 pages:1-14 https://dx.doi.org/10.1007/s11060-020-03394-y kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.81 ASE 44.90 ASE AR 147 2020 1 20 01 1-14 |
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Enthalten in Journal of neuro-oncology 147(2020), 1 vom: 20. Jan., Seite 1-14 volume:147 year:2020 number:1 day:20 month:01 pages:1-14 |
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Enthalten in Journal of neuro-oncology 147(2020), 1 vom: 20. Jan., Seite 1-14 volume:147 year:2020 number:1 day:20 month:01 pages:1-14 |
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Article |
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findex.gbv.de |
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Isocitrate dehydrogenase D2HG Telomerase Telomere length Q-FISH TERT promoter ALT ATRX |
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610 |
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Journal of neuro-oncology |
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Ferreira, Monica Sofia Ventura @@aut@@ Sørensen, Mia Dahl @@aut@@ Pusch, Stefan @@aut@@ Beier, Dagmar @@aut@@ Bouillon, Anne-Sophie @@aut@@ Kristensen, Bjarne Winther @@aut@@ Brümmendorf, Tim Henrik @@aut@@ Beier, Christoph Patrick @@aut@@ Beier, Fabian @@aut@@ |
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2020-01-20T00:00:00Z |
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32046122X |
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3610 |
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SPR039118487 |
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englisch |
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Depending on the IDH1 status, TERT promoter mutations affect prognosis. IDH1 mutations are associated with alpha-thalassemia/mental retardation syndrome X-linked (ATRX) mutations and alternative lengthening of telomeres (ALT), suggesting an interaction between IDH1 and telomeres. However, little is known how IDH1 mutations affect telomere maintenance. Methods We analyzed cell-specific telomere length (CS-TL) on a single cell level in 46 astrocytoma samples (WHO II-IV) by modified immune-quantitative fluorescence in situ hybridization, using endothelial cells as internal reference. In the same samples, we determined IDH1/TERT promoter mutation status and ATRX expression. The interaction of $ IDH1^{R132H} $ mutation and CS-TL was studied in vitro using an $ IDH1^{R132H} $ doxycycline-inducible glioma cell line system. Results Virtually all $ ALT^{positive} $ astrocytomas had normal TERT promoter and lacked ATRX expression. Further, all $ ALT^{positive} $ samples had $ IDH1^{R132H} $ mutations, resulting in a significantly longer CS-TL of $ IDH1^{R132H} $ gliomas, when compared to their wildtype counterparts. Conversely, TERT promotor mutations were associated with $ IDH^{wildtype} $, ATRX expression, lack of ALT and short CS-TL. ALT, TERT promoter mutations, and CS-TL remained without prognostic significance, when correcting for IDH1 status. In vitro, overexpression of $ IDH^{R132H} $ in the glioma cell line LN319 resulted in downregulation of ATRX and rapid TERT-independent telomere lengthening consistent with ALT. Conclusion ALT is the major telomere maintenance mechanism in $ IDH^{R132H} $ mutated astrocytomas, while TERT promoter mutations were associated with $ IDH^{wildtype} $ glioma. $ IDH1^{R132H} $ downregulates ATRX expression in vitro resulting in ALT, which may contribute to the strong association of $ IDH1^{R132H} $ mutations, ATRX loss, and ALT.</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Isocitrate dehydrogenase</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">D2HG</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Telomerase</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Telomere length</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Q-FISH</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">TERT promoter</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">ALT</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">ATRX</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Sørensen, Mia Dahl</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Pusch, Stefan</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Beier, Dagmar</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Bouillon, Anne-Sophie</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Kristensen, Bjarne Winther</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Brümmendorf, Tim Henrik</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Beier, Christoph Patrick</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Beier, Fabian</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="t">Journal of neuro-oncology</subfield><subfield code="d">Dordrecht [u.a.] : Springer Science + Business Media B.V, 1983</subfield><subfield code="g">147(2020), 1 vom: 20. 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|
| author |
Ferreira, Monica Sofia Ventura |
| spellingShingle |
Ferreira, Monica Sofia Ventura ddc 610 bkl 44.81 bkl 44.90 misc Isocitrate dehydrogenase misc D2HG misc Telomerase misc Telomere length misc Q-FISH misc TERT promoter misc ALT misc ATRX Alternative lengthening of telomeres is the major telomere maintenance mechanism in astrocytoma with isocitrate dehydrogenase 1 mutation |
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Ferreira, Monica Sofia Ventura |
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electronic Article |
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610 - Medicine & health |
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keep |
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aut aut aut aut aut aut aut aut aut |
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springer |
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true |
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Not Illustrated |
| issn |
1573-7373 |
| topic_title |
610 ASE 44.81 bkl 44.90 bkl Alternative lengthening of telomeres is the major telomere maintenance mechanism in astrocytoma with isocitrate dehydrogenase 1 mutation Isocitrate dehydrogenase (dpeaa)DE-He213 D2HG (dpeaa)DE-He213 Telomerase (dpeaa)DE-He213 Telomere length (dpeaa)DE-He213 Q-FISH (dpeaa)DE-He213 TERT promoter (dpeaa)DE-He213 ALT (dpeaa)DE-He213 ATRX (dpeaa)DE-He213 |
| topic |
ddc 610 bkl 44.81 bkl 44.90 misc Isocitrate dehydrogenase misc D2HG misc Telomerase misc Telomere length misc Q-FISH misc TERT promoter misc ALT misc ATRX |
| topic_unstemmed |
ddc 610 bkl 44.81 bkl 44.90 misc Isocitrate dehydrogenase misc D2HG misc Telomerase misc Telomere length misc Q-FISH misc TERT promoter misc ALT misc ATRX |
| topic_browse |
ddc 610 bkl 44.81 bkl 44.90 misc Isocitrate dehydrogenase misc D2HG misc Telomerase misc Telomere length misc Q-FISH misc TERT promoter misc ALT misc ATRX |
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Elektronische Aufsätze Aufsätze Elektronische Ressource |
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Journal of neuro-oncology |
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32046122X |
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610 - Medicine & health |
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Journal of neuro-oncology |
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true |
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(DE-627)32046122X (DE-600)2007293-4 |
| title |
Alternative lengthening of telomeres is the major telomere maintenance mechanism in astrocytoma with isocitrate dehydrogenase 1 mutation |
| ctrlnum |
(DE-627)SPR039118487 (SPR)s11060-020-03394-y-e |
| title_full |
Alternative lengthening of telomeres is the major telomere maintenance mechanism in astrocytoma with isocitrate dehydrogenase 1 mutation |
| author_sort |
Ferreira, Monica Sofia Ventura |
| journal |
Journal of neuro-oncology |
| journalStr |
Journal of neuro-oncology |
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eng |
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true |
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600 - Technology |
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marc |
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2020 |
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txt |
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1 |
| author_browse |
Ferreira, Monica Sofia Ventura Sørensen, Mia Dahl Pusch, Stefan Beier, Dagmar Bouillon, Anne-Sophie Kristensen, Bjarne Winther Brümmendorf, Tim Henrik Beier, Christoph Patrick Beier, Fabian |
| container_volume |
147 |
| class |
610 ASE 44.81 bkl 44.90 bkl |
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Elektronische Aufsätze |
| author-letter |
Ferreira, Monica Sofia Ventura |
| doi_str_mv |
10.1007/s11060-020-03394-y |
| dewey-full |
610 |
| author2-role |
verfasserin |
| title_sort |
alternative lengthening of telomeres is the major telomere maintenance mechanism in astrocytoma with isocitrate dehydrogenase 1 mutation |
| title_auth |
Alternative lengthening of telomeres is the major telomere maintenance mechanism in astrocytoma with isocitrate dehydrogenase 1 mutation |
| abstract |
Purpose Isocitrate dehydrogenase 1 (IDH1) mutations are associated with improved survival in gliomas. Depending on the IDH1 status, TERT promoter mutations affect prognosis. IDH1 mutations are associated with alpha-thalassemia/mental retardation syndrome X-linked (ATRX) mutations and alternative lengthening of telomeres (ALT), suggesting an interaction between IDH1 and telomeres. However, little is known how IDH1 mutations affect telomere maintenance. Methods We analyzed cell-specific telomere length (CS-TL) on a single cell level in 46 astrocytoma samples (WHO II-IV) by modified immune-quantitative fluorescence in situ hybridization, using endothelial cells as internal reference. In the same samples, we determined IDH1/TERT promoter mutation status and ATRX expression. The interaction of $ IDH1^{R132H} $ mutation and CS-TL was studied in vitro using an $ IDH1^{R132H} $ doxycycline-inducible glioma cell line system. Results Virtually all $ ALT^{positive} $ astrocytomas had normal TERT promoter and lacked ATRX expression. Further, all $ ALT^{positive} $ samples had $ IDH1^{R132H} $ mutations, resulting in a significantly longer CS-TL of $ IDH1^{R132H} $ gliomas, when compared to their wildtype counterparts. Conversely, TERT promotor mutations were associated with $ IDH^{wildtype} $, ATRX expression, lack of ALT and short CS-TL. ALT, TERT promoter mutations, and CS-TL remained without prognostic significance, when correcting for IDH1 status. In vitro, overexpression of $ IDH^{R132H} $ in the glioma cell line LN319 resulted in downregulation of ATRX and rapid TERT-independent telomere lengthening consistent with ALT. Conclusion ALT is the major telomere maintenance mechanism in $ IDH^{R132H} $ mutated astrocytomas, while TERT promoter mutations were associated with $ IDH^{wildtype} $ glioma. $ IDH1^{R132H} $ downregulates ATRX expression in vitro resulting in ALT, which may contribute to the strong association of $ IDH1^{R132H} $ mutations, ATRX loss, and ALT. |
| abstractGer |
Purpose Isocitrate dehydrogenase 1 (IDH1) mutations are associated with improved survival in gliomas. Depending on the IDH1 status, TERT promoter mutations affect prognosis. IDH1 mutations are associated with alpha-thalassemia/mental retardation syndrome X-linked (ATRX) mutations and alternative lengthening of telomeres (ALT), suggesting an interaction between IDH1 and telomeres. However, little is known how IDH1 mutations affect telomere maintenance. Methods We analyzed cell-specific telomere length (CS-TL) on a single cell level in 46 astrocytoma samples (WHO II-IV) by modified immune-quantitative fluorescence in situ hybridization, using endothelial cells as internal reference. In the same samples, we determined IDH1/TERT promoter mutation status and ATRX expression. The interaction of $ IDH1^{R132H} $ mutation and CS-TL was studied in vitro using an $ IDH1^{R132H} $ doxycycline-inducible glioma cell line system. Results Virtually all $ ALT^{positive} $ astrocytomas had normal TERT promoter and lacked ATRX expression. Further, all $ ALT^{positive} $ samples had $ IDH1^{R132H} $ mutations, resulting in a significantly longer CS-TL of $ IDH1^{R132H} $ gliomas, when compared to their wildtype counterparts. Conversely, TERT promotor mutations were associated with $ IDH^{wildtype} $, ATRX expression, lack of ALT and short CS-TL. ALT, TERT promoter mutations, and CS-TL remained without prognostic significance, when correcting for IDH1 status. In vitro, overexpression of $ IDH^{R132H} $ in the glioma cell line LN319 resulted in downregulation of ATRX and rapid TERT-independent telomere lengthening consistent with ALT. Conclusion ALT is the major telomere maintenance mechanism in $ IDH^{R132H} $ mutated astrocytomas, while TERT promoter mutations were associated with $ IDH^{wildtype} $ glioma. $ IDH1^{R132H} $ downregulates ATRX expression in vitro resulting in ALT, which may contribute to the strong association of $ IDH1^{R132H} $ mutations, ATRX loss, and ALT. |
| abstract_unstemmed |
Purpose Isocitrate dehydrogenase 1 (IDH1) mutations are associated with improved survival in gliomas. Depending on the IDH1 status, TERT promoter mutations affect prognosis. IDH1 mutations are associated with alpha-thalassemia/mental retardation syndrome X-linked (ATRX) mutations and alternative lengthening of telomeres (ALT), suggesting an interaction between IDH1 and telomeres. However, little is known how IDH1 mutations affect telomere maintenance. Methods We analyzed cell-specific telomere length (CS-TL) on a single cell level in 46 astrocytoma samples (WHO II-IV) by modified immune-quantitative fluorescence in situ hybridization, using endothelial cells as internal reference. In the same samples, we determined IDH1/TERT promoter mutation status and ATRX expression. The interaction of $ IDH1^{R132H} $ mutation and CS-TL was studied in vitro using an $ IDH1^{R132H} $ doxycycline-inducible glioma cell line system. Results Virtually all $ ALT^{positive} $ astrocytomas had normal TERT promoter and lacked ATRX expression. Further, all $ ALT^{positive} $ samples had $ IDH1^{R132H} $ mutations, resulting in a significantly longer CS-TL of $ IDH1^{R132H} $ gliomas, when compared to their wildtype counterparts. Conversely, TERT promotor mutations were associated with $ IDH^{wildtype} $, ATRX expression, lack of ALT and short CS-TL. ALT, TERT promoter mutations, and CS-TL remained without prognostic significance, when correcting for IDH1 status. In vitro, overexpression of $ IDH^{R132H} $ in the glioma cell line LN319 resulted in downregulation of ATRX and rapid TERT-independent telomere lengthening consistent with ALT. Conclusion ALT is the major telomere maintenance mechanism in $ IDH^{R132H} $ mutated astrocytomas, while TERT promoter mutations were associated with $ IDH^{wildtype} $ glioma. $ IDH1^{R132H} $ downregulates ATRX expression in vitro resulting in ALT, which may contribute to the strong association of $ IDH1^{R132H} $ mutations, ATRX loss, and ALT. |
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Alternative lengthening of telomeres is the major telomere maintenance mechanism in astrocytoma with isocitrate dehydrogenase 1 mutation |
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https://dx.doi.org/10.1007/s11060-020-03394-y |
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Sørensen, Mia Dahl Pusch, Stefan Beier, Dagmar Bouillon, Anne-Sophie Kristensen, Bjarne Winther Brümmendorf, Tim Henrik Beier, Christoph Patrick Beier, Fabian |
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Sørensen, Mia Dahl Pusch, Stefan Beier, Dagmar Bouillon, Anne-Sophie Kristensen, Bjarne Winther Brümmendorf, Tim Henrik Beier, Christoph Patrick Beier, Fabian |
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| doi_str |
10.1007/s11060-020-03394-y |
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2024-07-03T22:07:11.632Z |
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Depending on the IDH1 status, TERT promoter mutations affect prognosis. IDH1 mutations are associated with alpha-thalassemia/mental retardation syndrome X-linked (ATRX) mutations and alternative lengthening of telomeres (ALT), suggesting an interaction between IDH1 and telomeres. However, little is known how IDH1 mutations affect telomere maintenance. Methods We analyzed cell-specific telomere length (CS-TL) on a single cell level in 46 astrocytoma samples (WHO II-IV) by modified immune-quantitative fluorescence in situ hybridization, using endothelial cells as internal reference. In the same samples, we determined IDH1/TERT promoter mutation status and ATRX expression. The interaction of $ IDH1^{R132H} $ mutation and CS-TL was studied in vitro using an $ IDH1^{R132H} $ doxycycline-inducible glioma cell line system. Results Virtually all $ ALT^{positive} $ astrocytomas had normal TERT promoter and lacked ATRX expression. Further, all $ ALT^{positive} $ samples had $ IDH1^{R132H} $ mutations, resulting in a significantly longer CS-TL of $ IDH1^{R132H} $ gliomas, when compared to their wildtype counterparts. Conversely, TERT promotor mutations were associated with $ IDH^{wildtype} $, ATRX expression, lack of ALT and short CS-TL. ALT, TERT promoter mutations, and CS-TL remained without prognostic significance, when correcting for IDH1 status. In vitro, overexpression of $ IDH^{R132H} $ in the glioma cell line LN319 resulted in downregulation of ATRX and rapid TERT-independent telomere lengthening consistent with ALT. 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| score |
7.401639 |