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23 results on '"Thenoz Morgan"'

6. Pre-clinical evaluation of the hypomethylating agent decitabine for the treatment of t-cell lymphoblastic lymphoma

Author

Provez, Lien, Putteman, Tom, Landfors, Mattias, Roels, Juliette, Reunes, Lindy, T’Sas, Sara, Van Loocke, Wouter, Lintermans, Béatrice, De Coninck, Stien, Thenoz, Morgan, Sleeckx, Wouter, Maćkowska-Maślak, Natalia, Taghon, Tom, Mansour, Marc R., Farah, Nadine, Norga, Koen, Vandenberghe, Peter, Kotecha, Rishi S., Goossens, Steven, Degerman, Sofie, De Smedt, Renate, Van Vlierberghe, Pieter, Provez, Lien, Putteman, Tom, Landfors, Mattias, Roels, Juliette, Reunes, Lindy, T’Sas, Sara, Van Loocke, Wouter, Lintermans, Béatrice, De Coninck, Stien, Thenoz, Morgan, Sleeckx, Wouter, Maćkowska-Maślak, Natalia, Taghon, Tom, Mansour, Marc R., Farah, Nadine, Norga, Koen, Vandenberghe, Peter, Kotecha, Rishi S., Goossens, Steven, Degerman, Sofie, De Smedt, Renate, and Van Vlierberghe, Pieter

Abstract

T-cell lymphoblastic lymphoma (T-LBL) is a rare and aggressive lymphatic cancer, often diagnosed at a young age. Patients are treated with intensive chemotherapy, potentially followed by a hematopoietic stem cell transplantation. Although prognosis of T-LBL has improved with intensified treatment protocols, they are associated with side effects and 10–20% of patients still die from relapsed or refractory disease. Given this, the search toward less toxic anti-lymphoma therapies is ongoing. Here, we targeted the recently described DNA hypermethylated profile in T-LBL with the DNA hypomethylating agent decitabine. We evaluated the anti-lymphoma properties and downstream effects of decitabine, using patient derived xenograft (PDX) models. Decitabine treatment resulted in prolonged lymphoma-free survival in all T-LBL PDX models, which was associated with downregulation of the oncogenic MYC pathway. However, some PDX models showed more benefit of decitabine treatment compared to others. In more sensitive models, differentially methylated CpG regions resulted in more differentially expressed genes in open chromatin regions. This resulted in stronger downregulation of cell cycle genes and upregulation of immune response activating transcripts. Finally, we suggest a gene signature for high decitabine sensitivity in T-LBL. Altogether, we here delivered pre-clinical proof of the potential use of decitabine as a new therapeutic agent in T-LBL.

Published
2023
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7. Pre-Clinical Evaluation of the Hypomethylating Agent Decitabine for the Treatment of T-Cell Lymphoblastic Lymphoma

Author

Provez, Lien, primary, Putteman, Tom, additional, Landfors, Mattias, additional, Roels, Juliette, additional, Reunes, Lindy, additional, T’Sas, Sara, additional, Van Loocke, Wouter, additional, Lintermans, Béatrice, additional, De Coninck, Stien, additional, Thenoz, Morgan, additional, Sleeckx, Wouter, additional, Maćkowska-Maślak, Natalia, additional, Taghon, Tom, additional, Mansour, Marc R., additional, Farah, Nadine, additional, Norga, Koen, additional, Vandenberghe, Peter, additional, Kotecha, Rishi S., additional, Goossens, Steven, additional, Degerman, Sofie, additional, De Smedt, Renate, additional, and Van Vlierberghe, Pieter, additional

Published
2023
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11. Intragenic recruitment of NF-κB drives alternative splicing modifications upon activation by the viral oncogene TAX of HTLV-1

Author

Ameur, Lamya Ben, primary, Thenoz, Morgan, additional, Giraud, Guillaume, additional, Combe, Emmanuel, additional, Claude, Jean-Baptiste, additional, Lemaire, Sebastien, additional, Fontrodona, Nicolas, additional, Polveche, Hélène, additional, Bastien, Marine, additional, Gessain, Antoine, additional, Wattel, Eric, additional, Bourgeois, Cyril F., additional, Auboeuf, Didier, additional, and Mortreux, Franck, additional

Published
2019
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14. Oncogene- and drug resistance-associated alternative exon usage in acute myeloid leukemia (AML)

Author

Mohamed, Aminetou Mint, primary, Balsat, Marie, additional, Thenoz, Morgan, additional, Koering, Catherine, additional, Payen-Gay, Lea, additional, Cheok, Meyling, additional, Mortada, Hussein, additional, Auboeuf, Didier, additional, Pinatel, Christiane, additional, El-Hamri, Mohamed, additional, Dumontet, Charles, additional, Cros, Emeline, additional, Flandrin-Gresta, Pascale, additional, Nibourel, Olivier, additional, Preudhomme, Claude, additional, Michallet, Mauricette, additional, Thomas, Xavier, additional, Nicolini, Franck, additional, Solly, Françoise, additional, Guyotat, Denis, additional, Campos, Lydia, additional, Wattel, Eric, additional, and Mortreux, Franck, additional

Published
2015
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18. TET-catalyzed oxidation of intragenic 5-methylcytosine regulates CTCF-dependent alternative splicing.

Author

Marina, Ryan J, Sturgill, David, Bailly, Marc A, Thenoz, Morgan, Varma, Garima, Prigge, Maria F, Nanan, Kyster K, Shukla, Sanjeev, Haque, Nazmul, and Oberdoerffer, Shalini

Subjects
COMPLEMENTATION (Genetics), METHYLCYTOSINE, TRANSCRIPTIONAL repressor CTCF, ALTERNATIVE RNA splicing, RNA polymerase II
Abstract

Intragenic 5-methylcytosine and CTCF mediate opposing effects on pre- mRNA splicing: CTCF promotes inclusion of weak upstream exons through RNA polymerase II pausing, whereas 5-methylcytosine evicts CTCF, leading to exon exclusion. However, the mechanisms governing dynamic DNA methylation at CTCF-binding sites were unclear. Here, we reveal the methylcytosine dioxygenases TET1 and TET2 as active regulators of CTCF-mediated alternative splicing through conversion of 5-methylcytosine to its oxidation derivatives. 5-hydroxymethylcytosine and 5-carboxylcytosine are enriched at an intragenic CTCF-binding sites in the CD45 model gene and are associated with alternative exon inclusion. Reduced TET levels culminate in increased 5-methylcytosine, resulting in CTCF eviction and exon exclusion. In vitro analyses establish the oxidation derivatives are not sufficient to stimulate splicing, but efficiently promote CTCF association. We further show genomewide that reciprocal exchange of 5-hydroxymethylcytosine and 5-methylcytosine at downstream CTCF-binding sites is a general feature of alternative splicing in naïve and activated CD4+ T cells. These findings significantly expand our current concept of the pre- mRNA 'splicing code' to include dynamic intragenic DNA methylation catalyzed by the TET proteins. [ABSTRACT FROM AUTHOR]

Published
2016
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19. DEK and WT1 Affect Alternative Splicing of Genes Involved in Hematopoietic Cell Lineage and Resistance to Chemotherapy in Acute Myeloid Leukemia Cells.

Author

Mohamed, Aminetou Mint, primary, Thenoz, Morgan, additional, Koering, Catherine, additional, Mallinjoud, Pierre, additional, Auboeuf, Didier, additional, Solly, Francoise, additional, Cheok, Meyling, additional, Nibourel, Olivier, additional, Preudhomme, Claude, additional, Wattel, Eric, additional, and Mortreux, Franck, additional

Published
2012
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22. Skipping of ATP-Binding Cassette Transporter A3 Exon 19 in AML Cells Is an Independent Prognostic Factor in Patients with Normal Cytogenetics

Author

Mohamed, Aminetou Mint, Thenoz, Morgan, Payen-Gay, Lea, Maucort-Boulch, Delphine, Mortada, Hussein, Auboeuf, Didier, Koering, Catherine, Cheok, Meyling, Nibourel, Olivier, Preudhomme, Claude, El-Hamri, Mohamed, Thomas, Xavier, Nicolini, Franck E., Tigaud, Isabelle, Cros, Emeline, Dumontet, Charles, Campos, Lydia, Solly, Francoise, Guyotat, Denis, Flandrin-Gresta, Pascale, Mortreux, Franck, and Wattel, Eric

Published
2014
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23. Oncogene- and drug resistance-associated alternative exon usage in acute myeloid leukemia (AML).

Author

Mohamed AM, Balsat M, Thenoz M, Koering C, Payen-Gay L, Cheok M, Mortada H, Auboeuf D, Pinatel C, El-Hamri M, Dumontet C, Cros E, Flandrin-Gresta P, Nibourel O, Preudhomme C, Michallet M, Thomas X, Nicolini F, Solly F, Guyotat D, Campos L, Wattel E, and Mortreux F

Subjects
Aged, Anthracyclines pharmacology, Azacitidine pharmacology, Cell Line, Tumor, Chromosomal Proteins, Non-Histone metabolism, Cytarabine pharmacology, Doxorubicin pharmacology, Exons genetics, Gene Expression Profiling, HEK293 Cells, Humans, Male, Middle Aged, Oncogene Proteins metabolism, Oncogenes genetics, Poly-ADP-Ribose Binding Proteins, RNA Interference, RNA, Small Interfering genetics, WT1 Proteins metabolism, Alternative Splicing genetics, Antineoplastic Agents pharmacology, Drug Resistance, Neoplasm genetics, Leukemia, Myeloid, Acute drug therapy, Leukemia, Myeloid, Acute genetics
Abstract

In addition to spliceosome gene mutations, oncogene expression and drug resistance in AML might influence exon expression. We performed exon-array analysis and exon-specific PCR (ESPCR) to identify specific landscapes of exon expression that are associated with DEK and WT1 oncogene expression and the resistance of AML cells to AraC, doxorubicin or azacitidine. Data were obtained for these five conditions through exon-array analysis of 17 cell lines and 24 patient samples and were extended through qESPCR of samples from 152 additional AML cases. More than 70% of AEUs identified by exon-array were technically validated through ESPCR. In vitro, 1,130 to 5,868 exon events distinguished the 5 conditions from their respective controls while in vivo 6,560 and 9,378 events distinguished chemosensitive and chemoresistant AML, respectively, from normal bone marrow. Whatever the cause of this effect, 30 to 80% of mis-spliced mRNAs involved genes unmodified at the whole transcriptional level. These AEUs unmasked new functional pathways that are distinct from those generated by transcriptional deregulation. These results also identified new putative pathways that could help increase the understanding of the effects mediated by DEK or WT1, which may allow the targeting of these pathways to prevent resistance of AML cells to chemotherapeutic agents.

Published
2016
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