BET protein inhibition sensitizes glioblastoma cells to temozolomide treatment by attenuating MGMT expression
- Location
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Deutsche Nationalbibliothek Frankfurt am Main
- ISSN
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2041-4889
- Extent
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Online-Ressource
- Language
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Englisch
- Notes
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online resource.
- Bibliographic citation
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BET protein inhibition sensitizes glioblastoma cells to temozolomide treatment by attenuating MGMT expression ; volume:13 ; number:12 ; day:13 ; month:12 ; year:2022 ; pages:1-12 ; date:12.2022
Cell death & disease ; 13, Heft 12 (13.12.2022), 1-12, 12.2022
- Creator
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Tancredi, Alessandro
Gusyatiner, Olga
Bady, Pierre
Buri, Michelle C.
Lomazzi, Rémy
Chiesi, Davide
Messerer, Mahmoud
Hegi, Monika E.
- Contributor
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SpringerLink (Online service)
- DOI
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10.1038/s41419-022-05497-y
- URN
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urn:nbn:de:101:1-2023022221143499267116
- Rights
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Open Access; Der Zugriff auf das Objekt ist unbeschränkt möglich.
- Last update
-
14.08.2025, 10:51 AM CEST
Data provider
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Deutsche Nationalbibliothek. If you have any questions about the object, please contact the data provider.
Associated
- Tancredi, Alessandro
- Gusyatiner, Olga
- Bady, Pierre
- Buri, Michelle C.
- Lomazzi, Rémy
- Chiesi, Davide
- Messerer, Mahmoud
- Hegi, Monika E.
- SpringerLink (Online service)
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Fstl1/DIP2A/MGMT signaling pathway plays important roles in temozolomide resistance in glioblastoma
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Epigenetic preconditioning with decitabine sensitizes glioblastoma to temozolomide via induction of MLH1
Hedgehog/Gli1 signaling pathway regulates MGMT expression and chemoresistance to temozolomide in human glioblastoma
MGMT promoter methylation status and MGMT and CD133 immunohistochemical expression as prognostic markers in glioblastoma patients treated with temozolomide plus radiotherapy
Overexpression miR-486-3p Promoted by Allicin Enhances Temozolomide Sensitivity in Glioblastoma Via Targeting MGMT
Combination chemotherapy versus temozolomide for patients with methylated MGMT (m-MGMT) glioblastoma: results of computational biological modeling to predict the magnitude of treatment benefit
Prognostic value of TP53 expression and MGMT methylation in glioblastoma patients treated with temozolomide combined with other chemotherapies
Stanniocalcin-1 promotes temozolomide resistance of glioblastoma through regulation of MGMT
Mitochondria‐Targeted Temozolomide Probe for Overcoming MGMT‐Mediated Resistance in Glioblastoma
Inhibition of gap junctions sensitizes primary glioblastoma cells for temozolomide
A novel enhancer regulates MGMT expression and promotes temozolomide resistance in glioblastoma
Fstl1/DIP2A/MGMT signaling pathway plays important roles in temozolomide resistance in glioblastoma
Ibudilast sensitizes glioblastoma to temozolomide by targeting Macrophage Migration Inhibitory Factor (MIF)
Epigenetic preconditioning with decitabine sensitizes glioblastoma to temozolomide via induction of MLH1
Hedgehog/Gli1 signaling pathway regulates MGMT expression and chemoresistance to temozolomide in human glioblastoma
MGMT promoter methylation status and MGMT and CD133 immunohistochemical expression as prognostic markers in glioblastoma patients treated with temozolomide plus radiotherapy
Overexpression miR-486-3p Promoted by Allicin Enhances Temozolomide Sensitivity in Glioblastoma Via Targeting MGMT
Combination chemotherapy versus temozolomide for patients with methylated MGMT (m-MGMT) glioblastoma: results of computational biological modeling to predict the magnitude of treatment benefit
Prognostic value of TP53 expression and MGMT methylation in glioblastoma patients treated with temozolomide combined with other chemotherapies
Stanniocalcin-1 promotes temozolomide resistance of glioblastoma through regulation of MGMT
Mitochondria‐Targeted Temozolomide Probe for Overcoming MGMT‐Mediated Resistance in Glioblastoma
Inhibition of gap junctions sensitizes primary glioblastoma cells for temozolomide
A novel enhancer regulates MGMT expression and promotes temozolomide resistance in glioblastoma
Fstl1/DIP2A/MGMT signaling pathway plays important roles in temozolomide resistance in glioblastoma
Ibudilast sensitizes glioblastoma to temozolomide by targeting Macrophage Migration Inhibitory Factor (MIF)
Epigenetic preconditioning with decitabine sensitizes glioblastoma to temozolomide via induction of MLH1
Hedgehog/Gli1 signaling pathway regulates MGMT expression and chemoresistance to temozolomide in human glioblastoma
MGMT promoter methylation status and MGMT and CD133 immunohistochemical expression as prognostic markers in glioblastoma patients treated with temozolomide plus radiotherapy
Overexpression miR-486-3p Promoted by Allicin Enhances Temozolomide Sensitivity in Glioblastoma Via Targeting MGMT
Combination chemotherapy versus temozolomide for patients with methylated MGMT (m-MGMT) glioblastoma: results of computational biological modeling to predict the magnitude of treatment benefit