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6 results on '"Soulier, J. (Jean)"'

1. ZEB2 drives immature T-cell lymphoblastic leukaemia development via enhanced tumour-initiating potential and IL-7 receptor signalling

Author

Goossens, S. (Steven), Radaelli, E. (Enrico), Blanchet, O. (Odile), Durinck, K. (Kaat), Meulen, J. (Joni) van der, Peirs, S. (Sofie), Taghon, T. (Tom), Tremblay, C.S. (Cedric S.), Costa, M. (Magdaline), Ghahremani, M.F., De Medts, J. (Jelle), Bartunkova, S. (Sonia), Haigh, K. (Katharina), Schwab, C. (Claire), Farla, N. (Natalie), Pieters, T. (Tim), Matthijssens, F. (Filip), Roy, N. (Nadine) van, Best, J.A. (J. Adam), Deswarte, K. (Kim), Bogaert, P. (Pieter), Carmichael, C. (Catherine), Rickard, A. (Adam), Suryani, S. (Santi), Bracken, L.S. (Lauryn S.), Alserihi, R. (Raed), Canté-Barrett, K. (Kirsten), Haenebalcke, L. (Lieven), Clappier, E., Rondou, P. (Pieter), Slowicka, K. (Karolina), Huylebroeck, D. (Danny), Goldrath, A.W. (Ananda W.), Janzen, V. (Viktor), McCormack, M.P. (Matthew P.), Lock, R.B. (Richard B.), Curtis, D.J. (David J.), Harrison, C.J. (Christine), Berx, G. (Geert), Speleman, F. (Franki), Meijerink, J.P.P. (Jules), Soulier, J. (Jean), Vlierberghe, P. (Pieter) van, Goossens, S. (Steven), Radaelli, E. (Enrico), Blanchet, O. (Odile), Durinck, K. (Kaat), Meulen, J. (Joni) van der, Peirs, S. (Sofie), Taghon, T. (Tom), Tremblay, C.S. (Cedric S.), Costa, M. (Magdaline), Ghahremani, M.F., De Medts, J. (Jelle), Bartunkova, S. (Sonia), Haigh, K. (Katharina), Schwab, C. (Claire), Farla, N. (Natalie), Pieters, T. (Tim), Matthijssens, F. (Filip), Roy, N. (Nadine) van, Best, J.A. (J. Adam), Deswarte, K. (Kim), Bogaert, P. (Pieter), Carmichael, C. (Catherine), Rickard, A. (Adam), Suryani, S. (Santi), Bracken, L.S. (Lauryn S.), Alserihi, R. (Raed), Canté-Barrett, K. (Kirsten), Haenebalcke, L. (Lieven), Clappier, E., Rondou, P. (Pieter), Slowicka, K. (Karolina), Huylebroeck, D. (Danny), Goldrath, A.W. (Ananda W.), Janzen, V. (Viktor), McCormack, M.P. (Matthew P.), Lock, R.B. (Richard B.), Curtis, D.J. (David J.), Harrison, C.J. (Christine), Berx, G. (Geert), Speleman, F. (Franki), Meijerink, J.P.P. (Jules), Soulier, J. (Jean), and Vlierberghe, P. (Pieter) van

Abstract

Early T-cell precursor leukaemia (ETP-ALL) is a high-risk subtype of human leukaemia that is poorly understood at the molecular level. Here we report translocations targeting the zinc finger E-box-binding transcription factor ZEB2 as a recurrent genetic lesion in immature/ETP-ALL. Using a conditional gain-of-function mouse model, we demonstrate that sustained Zeb2 expression initiates T-cell leukaemia. Moreover, Zeb2-driven mouse leukaemia exhibit some features of the human immature/ETP-ALL gene expression signature, as well as an enhanced leukaemia-initiation potential and activated Janus kinase (JAK)/signal transducers and activators of transcription (STAT) signalling through transcriptional activation of IL7R. This study reveals ZEB2 as an oncogene in the biology of immature/ETP-ALL and paves the way towards pre-clinical studies of novel compounds for the treatment of this aggressive subtype of human T-ALL using our Zeb2-driven mouse model.

Published
2015
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2. Posttranscriptional deregulation of MYC via PTEN constitutes a major alternative pathway of MYC activation in T-cell acute lymphoblastic leukemia

Author

Bonnet, M. (Mélanie), Loosveld, M. (Marie), Montpellier, B. (Bertrand), Navarro, J.-M., Quilichini, B. (Benoit), Picard, C. (Christophe), Cristofaro, J.D., Bagnis, C. (Claude), Fossat, C. (Chantal), Hernandez, L. (Lucie), Mamessier, E. (Emilie), Roulland, S. (Sandrine), Morgado, E. (Ester), Formisano-Tréziny, C. (Christine), Dik, W.A. (Willem), Langerak, A.W. (Anton), Prebet, T. (Thomas), Vey, N. (Norbert), Michel, G. (Gérard), Gabert, J. (Jean), Soulier, J. (Jean), Macintyre, E., Asnafi, V. (Vahid), Payet-Bornet, D. (Dominique), Nadel, B. (Bertrand), Bonnet, M. (Mélanie), Loosveld, M. (Marie), Montpellier, B. (Bertrand), Navarro, J.-M., Quilichini, B. (Benoit), Picard, C. (Christophe), Cristofaro, J.D., Bagnis, C. (Claude), Fossat, C. (Chantal), Hernandez, L. (Lucie), Mamessier, E. (Emilie), Roulland, S. (Sandrine), Morgado, E. (Ester), Formisano-Tréziny, C. (Christine), Dik, W.A. (Willem), Langerak, A.W. (Anton), Prebet, T. (Thomas), Vey, N. (Norbert), Michel, G. (Gérard), Gabert, J. (Jean), Soulier, J. (Jean), Macintyre, E., Asnafi, V. (Vahid), Payet-Bornet, D. (Dominique), and Nadel, B. (Bertrand)

Abstract

Cumulative evidence indicates that MYC, one of the major downstream effectors of NOTCH1, is a critical component of T-cell acute lymphoblastic leukemia (T-ALL) oncogenesis and a potential candidate for targeted therapy. However, MYC is a complex oncogene, involving both fine protein dosage and cell-context dependency, and detailed understanding of MYC-mediated oncogenesis in T-ALL is still lacking. To better understand how MYC is interspersed in the complex T-ALL oncogenic networks, we performed a thorough molecular and biochemical analysis of MYC activation in a comprehensive collection of primary adult and pediatric patient samples. We find that MYC expression is highly variable, and that high MYC expression levels can be generated in a large number of cases in absence of NOTCH1/FBXW7 mutations, suggesting the occurrence of multiple activation pathways in addition to NOTCH1. Furthermore, we show that posttranscriptional deregulation of MYC constitutes a major alternative pathway of MYC activation in T-ALL, operating partly via the PI3K/AKT axis through down-regulation of PTEN, and that NOTCH1mmight play a dual transcriptional and posttranscriptional role in this process. Altogether, our data lend further support to the significance of therapeutic targeting of MYC and/or the PTEN/AKT pathways, both in GSI-resistant and identified NOTCH1-independent/MYC-mediated T-ALL patients.

Published
2011
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3. PTPN2 negatively regulates oncogenic JAK1 in T-cell acute lymphoblastic leukemia

Author

Kleppe, M. (Maria), Soulier, J. (Jean), Asnafi, V. (Vahid), Mentens, N. (Nicole), Hornakova, T. (Tekla), Knoops, L. (Laurent), Constantinescu, S. (Stefan), Sigaux, F. (François), Meijerink, J.P.P. (Jules), Vandenberghe, P. (Peter), Tartaglia, M. (Marco), Foà, R. (Robin), Macintyre, E., Haferlach, T. (Torsten), Cools, J. (Jan), Kleppe, M. (Maria), Soulier, J. (Jean), Asnafi, V. (Vahid), Mentens, N. (Nicole), Hornakova, T. (Tekla), Knoops, L. (Laurent), Constantinescu, S. (Stefan), Sigaux, F. (François), Meijerink, J.P.P. (Jules), Vandenberghe, P. (Peter), Tartaglia, M. (Marco), Foà, R. (Robin), Macintyre, E., Haferlach, T. (Torsten), and Cools, J. (Jan)

Abstract

We have recently reported inactivation of the tyrosine phosphatase PTPN2 (also known as TC-PTP) through deletion of the entire gene locus in ∼ 6% of T-cell acute lymphoblastic leukemia (T-ALL) cases. T-ALL is an aggressive disease of the thymocytes characterized by the stepwise accumulation of chromosomal abnormalities and gene mutations. In the present study, we confirmed the strong association of the PTPN2 deletion with TLX1 and NUP214-ABL1 expression. In addition, we found cooperation between PTPN2 deletion and activating JAK1 gene mutations. Activating mutations in JAK1 kinase occur in ∼ 10% of human T-ALL cases, and aberrant kinase activity has been shown to confer proliferation and survival advantages. Our results reveal that some JAK1 mutation - positive TALLs harbor deletions of the tyrosine phosphatase PTPN2, a known negative regulator of the JAK/STAT pathway. We provide evidence that down-regulation of Ptpn2 sensitizes lymphoid cells to JAK1-mediated transformation and reduces their sensitivity to JAK inhibition.

Published
2011
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4. The TLX1 oncogene drives aneuploidy in T cell transformation

Author

Keersmaecker, K. (Kim) de, Real, P.J. (Pedro), Gatta, G.D., Palomero, T. (Teresa), Sulis, M.L., Tosello, V. (Valeria), Vlierberghe, P. (Pieter) van, Barnes, K. (Kelly), Castillo, M. (Mireia), Sole, X. (Xavier), Hadler, M. (Michael), Lenz, J. (Jack), Aplan, P.D. (Peter), Kelliher, M. (Michelle), Kee, B.L. (Barbara), Pandolfi, P.P., Kappes, D. (Dietmar), Gounari, F. (Fotini), Petrie, H. (Howard), Meulen, J. (Joni) van der, Speleman, F. (Franki), Paietta, E. (Elisabeth), Racevskis, J. (Janis), Wiernik, P.H. (Peter), Rowe, J. (Jacob), Soulier, J. (Jean), Avran, D. (David), Cavé, H. (Hélène), Dastugue, N. (Nicole), Raimondi, S. (Susana), Meijerink, J.P.P. (Jules), Cordon-Cardo, C. (Carlos), Califano, A. (Andrea), Ferrando, A.A. (Adolfo), Keersmaecker, K. (Kim) de, Real, P.J. (Pedro), Gatta, G.D., Palomero, T. (Teresa), Sulis, M.L., Tosello, V. (Valeria), Vlierberghe, P. (Pieter) van, Barnes, K. (Kelly), Castillo, M. (Mireia), Sole, X. (Xavier), Hadler, M. (Michael), Lenz, J. (Jack), Aplan, P.D. (Peter), Kelliher, M. (Michelle), Kee, B.L. (Barbara), Pandolfi, P.P., Kappes, D. (Dietmar), Gounari, F. (Fotini), Petrie, H. (Howard), Meulen, J. (Joni) van der, Speleman, F. (Franki), Paietta, E. (Elisabeth), Racevskis, J. (Janis), Wiernik, P.H. (Peter), Rowe, J. (Jacob), Soulier, J. (Jean), Avran, D. (David), Cavé, H. (Hélène), Dastugue, N. (Nicole), Raimondi, S. (Susana), Meijerink, J.P.P. (Jules), Cordon-Cardo, C. (Carlos), Califano, A. (Andrea), and Ferrando, A.A. (Adolfo)

Abstract

The TLX1 oncogene (encoding the transcription factor T cell leukemia homeobox protein-1) has a major role in the pathogenesis of T cell acute lymphoblastic leukemia (T-ALL). However, the specific mechanisms of T cell transformation downstream of TLX1 remain to be elucidated. Here we show that transgenic expression of human TLX1 in mice induces T-ALL with frequent deletions and mutations in Bcl11b (encoding B cell leukemia/lymphoma-11B) and identify the presence of recurrent mutations and deletions in BCL11B in 16% of human T-ALLs. Most notably, mouse TLX1 tumors were typically aneuploid and showed a marked defect in the activation of the mitotic checkpoint. Mechanistically, TLX1 directly downregulates the expression of CHEK1 (encoding CHK1 checkpoint homolog) and additional mitotic control genes and induces loss of the mitotic checkpoint in nontransformed preleukemic thymocytes. These results identify a previously unrecognized mechanism contributing to chromosomal missegregation and aneuploidy active at the earliest stages of tumor development in the pathogenesis of cancer.

Published
2010
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5. PHF6 mutations in T-cell acute lymphoblastic leukemia

Author

Vlierberghe, P. (Pieter) van, Palomero, T. (Teresa), Khiabanian, H. (Hossein), Meulen, J. (Joni) van der, Castillo, M. (Mireia), Roy, N. (Nadine) van, Moerloose, B. (Barbara) de, Philippé, J. (Jan), González-García, S. (Sara), Toribio, M.L. (María), Taghon, T. (Tom), Zuurbier, L.C. (Linda), Cauwelier, B. (Barbara), Harrison, C.J. (Christine), Schwab, C. (Claire), Pisecker, M. (Markus), Strehl, S., Langerak, A.W. (Anton), Gecz, J. (Jozef), Sonneveld, E. (Edwin), Pieters, R. (Rob), Paietta, E. (Elisabeth), Rowe, J. (Jacob), Wiernik, P.H. (Peter), Benoit, Y. (Yves), Soulier, J. (Jean), Poppe, B. (Bruce), Yao, X. (Xiaopan), Cordon-Cardo, C. (Carlos), Meijerink, J.P.P. (Jules), Rabadan, R. (Raul), Speleman, F. (Franki), Ferrando, A.A. (Adolfo), Vlierberghe, P. (Pieter) van, Palomero, T. (Teresa), Khiabanian, H. (Hossein), Meulen, J. (Joni) van der, Castillo, M. (Mireia), Roy, N. (Nadine) van, Moerloose, B. (Barbara) de, Philippé, J. (Jan), González-García, S. (Sara), Toribio, M.L. (María), Taghon, T. (Tom), Zuurbier, L.C. (Linda), Cauwelier, B. (Barbara), Harrison, C.J. (Christine), Schwab, C. (Claire), Pisecker, M. (Markus), Strehl, S., Langerak, A.W. (Anton), Gecz, J. (Jozef), Sonneveld, E. (Edwin), Pieters, R. (Rob), Paietta, E. (Elisabeth), Rowe, J. (Jacob), Wiernik, P.H. (Peter), Benoit, Y. (Yves), Soulier, J. (Jean), Poppe, B. (Bruce), Yao, X. (Xiaopan), Cordon-Cardo, C. (Carlos), Meijerink, J.P.P. (Jules), Rabadan, R. (Raul), Speleman, F. (Franki), and Ferrando, A.A. (Adolfo)

Abstract

Tumor suppressor genes on the X chromosome may skew the gender distribution of specific types of cancer. T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive hematological malignancy with an increased incidence in males. In this study, we report the identification of inactivating mutations and deletions in the X-linked plant homeodomain finger 6 (PHF6) gene in 16% of pediatric and 38% of adult primary T-ALL samples. Notably, PHF6 mutations are almost exclusively found in T-ALL samples from male subjects. Mutational loss of PHF6 is importantly associated with leukemias driven by aberrant expression of the homeobox transcription factor oncogenes TLX1 and TLX3. Overall, these results identify PHF6 as a new X-linked tumor suppressor in T-ALL and point to a strong genetic interaction between PHF6 loss and aberrant expression of TLX transcription factors in the pathogenesis of this disease.

Published
2010
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6. The recurrent SET-NUP214 fusion as a new HOXA activation mechanism in pediatric T-cell acute lymphoblastic leukemia

Author

Vlierberghe, P. (Pieter) van, Grotel, M. (Martine) van, Tchinda, J. (Joëlle), Lee, C. (Charles), Beverloo, H.B. (Berna), Spek, P.J. (Peter) van der, Stubbs, A.P. (Andrew), Cools, J. (Jan), Nagata, K. (Kyosuke), Fornerod, M.W.J. (Maarten), Buijs-Gladdines, J.G.C.A.M. (Jessica), Horstmann, M.A. (Martin), Wering, E.R. (Elisabeth) van, Soulier, J. (Jean), Pieters, R. (Rob), Meijerink, J.P.P. (Jules), Vlierberghe, P. (Pieter) van, Grotel, M. (Martine) van, Tchinda, J. (Joëlle), Lee, C. (Charles), Beverloo, H.B. (Berna), Spek, P.J. (Peter) van der, Stubbs, A.P. (Andrew), Cools, J. (Jan), Nagata, K. (Kyosuke), Fornerod, M.W.J. (Maarten), Buijs-Gladdines, J.G.C.A.M. (Jessica), Horstmann, M.A. (Martin), Wering, E.R. (Elisabeth) van, Soulier, J. (Jean), Pieters, R. (Rob), and Meijerink, J.P.P. (Jules)

Abstract

T-cell acute lymphoblastic leukemia (TALL) is mostly characterized by specific chromosomal abnormalities, some occurring in a mutually exclusive manner that possibly delineate specific T-ALL subgroups. One subgroup, including MLLrearranged, CALM-AFWor inv (7)(p15q34) patients, is characterized by elevated expression of HOXA genes. Using a gene expression-based clustering analysis of 67

Published
2008
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