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25 results on '"Kosasih, Hansen J."'

1. The third generation AKR1C3-activated prodrug, ACHM-025, eradicates disease in preclinical models of aggressive T-cell acute lymphoblastic leukemia

Author

Toscan, Cara E., McCalmont, Hannah, Ashoorzadeh, Amir, Lin, Xiaojing, Fu, Zhe, Doculara, Louise, Kosasih, Hansen J., Cadiz, Roxanne, Zhou, Anthony, Williams, Sarah, Evans, Kathryn, Khalili, Faezeh, Cai, Ruilin, Yeats, Kristy L., Gifford, Andrew J., Pickford, Russell, Mayoh, Chelsea, Xie, Jinhan, Henderson, Michelle J., Trahair, Toby N., Patterson, Adam V., Smaill, Jeff B., de Bock, Charles E., and Lock, Richard B.

Published
2024
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2. PU.1 eviction at lymphocyte-specific chromatin domains mediates glucocorticoid response in acute lymphoblastic leukemia

Author

Beck, Dominik, Cao, Honghui, Tian, Feng, Huang, Yizhou, Jiang, Miao, Zhao, Han, Tai, Xiaolu, Xu, Wenqian, Kosasih, Hansen J., Kealy, David J., Zhao, Weiye, Taylor, Samuel J., Couttas, Timothy A., Song, Gaoxian, Chacon-Fajardo, Diego, Walia, Yashna, Wang, Meng, Dowle, Adam A., Holding, Andrew N., Bridge, Katherine S., Zhang, Chao, Wang, Jin, Mi, Jian-Qing, Lock, Richard B., de Bock, Charles E., and Jing, Duohui

Published
2024
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8. A novel MYB::PAIP1 oncogenic fusion in pediatric blastic plasmacytoid dendritic cell neoplasm (BPDCN) is dependent on BCL2 expression and is sensitive to venetoclax

Author

Kosasih, Hansen J., primary, Healey, Gerry, additional, Brennan, Margs S., additional, Bjelosevic, Stefan, additional, Sadras, Teresa, additional, Jalud, Fatimah B., additional, Ibnat, Tasnia, additional, Ng, Ashley P., additional, Mayoh, Chelsea, additional, Mao, Jie, additional, Tax, Gabor, additional, Ludlow, Louise E. A., additional, Johnstone, Ricky W., additional, Herold, Marco J., additional, Khaw, Seong L., additional, de Bock, Charles E., additional, and Ekert, Paul G., additional

Published
2024
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10. Human MLL/KMT2A gene exhibits a second breakpoint cluster region for recurrent MLL–USP2 fusions

Author

Meyer, Claus, Lopes, Bruno A., Caye-Eude, Aurélie, Cavé, Hélène, Arfeuille, Chloé, Cuccuini, Wendy, Sutton, Rosemary, Venn, Nicola C., Oh, Seung Hwan, Tsaur, Grigory, Escherich, Gabriele, Feuchtinger, Tobias, Kosasih, Hansen J., Khaw, Seong L., Ekert, Paul G., Pombo-de-Oliveira, Maria S., Bidet, Audrey, Djahanschiri, Bardya, Ebersberger, Ingo, Zaliova, Marketa, Zuna, Jan, Zermanova, Zuzana, Juvonen, Vesa, Grümayer, Renate Panzer, Fazio, Grazia, Cazzaniga, Gianni, Larghero, Patrizia, Emerenciano, Mariana, and Marschalek, Rolf

Published
2019
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11. Targeting hyperactive platelet-derived growth factor receptor-β signaling in T-cell acute lymphoblastic leukemia and lymphoma

Author

De Coninck, Stien, primary, De Smedt, Renate, additional, Lintermans, Beatrice, additional, Reunes, Lindy, additional, Kosasih, Hansen J., additional, Reekmans, Alexandra, additional, Brown, Lauren M., additional, Van Roy, Nadine, additional, Palhais, Bruno, additional, Roels, Juliette, additional, Van der Linden, Malaika, additional, Van Dorpe, Jo, additional, Ntziachristos, Panagiotis, additional, Van Delft, Frederik W., additional, Mansour, Marc R., additional, Pieters, Tim, additional, Lammens, Tim, additional, De Moerloose, Barbara, additional, De Bock, Charles E., additional, Goossens, Steven, additional, and Van Vlierberghe, Pieter, additional

Published
2023
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13. In vitro and in vivo modelling of mutant JAK3/STAT5 signaling in leukemia

Author

Omari, Sofia A, Kosasih, Hansen J ; https://orcid.org/0000-0002-0428-6195, Chung, Thomas, de Bock, Charles E ; https://orcid.org/0000-0001-5182-8535, Omari, Sofia A, Kosasih, Hansen J ; https://orcid.org/0000-0002-0428-6195, Chung, Thomas, and de Bock, Charles E ; https://orcid.org/0000-0001-5182-8535

Abstract

Mutations within the IL7-R-JAK-STAT signaling pathway are important drivers of T-cell acute lymphoblastic leukemia (T-ALL). Here we describe the important steps required to generate retroviral particles for the stable expression of mutant JAK3 constructs that induce constitutive JAK/STAT signaling. These are subsequently used for the viral transduction of the IL-3 cytokine-dependent Ba/F3 cell line or murine hematopoietic stem and progenitor cells (HSPCs) for in vitro and in vivo modelling of cytokine-independent growth or leukemia initiation respectively.

Published
2023

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Author

De Coninck, Stien, De Smedt, Renate, Lintermans, Beatrice, Reunes, Lindy, Kosasih, Hansen J ; https://orcid.org/0000-0002-0428-6195, Reekmans, Alexandra, Brown, Lauren M ; https://orcid.org/0000-0002-4322-8203, Van Roy, Nadine, Palhais, Bruno, Roels, Juliette, Van der Linden, Malaika, Van Dorpe, Jo, Ntziachristos, Panagiotis, Van Delft, Frederik W, Mansour, Marc R, Pieters, Tim, Lammens, Tim, De Moerloose, Barbara, De Bock, Charles E ; https://orcid.org/0000-0001-5182-8535, Goossens, Steven, Van Vlierberghe, Pieter, De Coninck, Stien, De Smedt, Renate, Lintermans, Beatrice, Reunes, Lindy, Kosasih, Hansen J ; https://orcid.org/0000-0002-0428-6195, Reekmans, Alexandra, Brown, Lauren M ; https://orcid.org/0000-0002-4322-8203, Van Roy, Nadine, Palhais, Bruno, Roels, Juliette, Van der Linden, Malaika, Van Dorpe, Jo, Ntziachristos, Panagiotis, Van Delft, Frederik W, Mansour, Marc R, Pieters, Tim, Lammens, Tim, De Moerloose, Barbara, De Bock, Charles E ; https://orcid.org/0000-0001-5182-8535, Goossens, Steven, and Van Vlierberghe, Pieter

Abstract

T cell acute lymphoblastic leukemia (T-ALL) and T cell lymphoblastic lymphoma (T-LBL) are rare aggressive hematological malignancies. Current treatment consists of intensive chemotherapy, leading to 80% overall survival but are associated with severe toxic side effects. Furthermore, 10-20% of patients still die from relapsed or refractory disease providing a strong rationale for more specific, targeted therapeutic strategies with less toxicities. Here, we report a novel MYH9::PDGFRB fusion in a T-LBL patient and demonstrate that this fusion product is constitutively active and sufficient to drive oncogenic transformation in vitro and in vivo. Expanding our analysis more broadly across T-ALL, we found a T-ALL cell line and multiple patient derived xenograft models with PDGFRB hyperactivation in the absence of a fusion, with high PDGFRB expression in TLX3 and HOXA T-ALL molecular subtypes. To target this PDGFRB hyperactivation, we evaluated the therapeutic effects of a selective PDGFRB inhibitor, CP-673451, both in vitro and in vivo and demonstrated sensitivity if the receptor is hyperactivated. Altogether, our work reveals that hyperactivation of PDGFRB is an oncogenic driver in T-ALL/T-LBL and that screening T-ALL/TLBL patients for phosphorylated PDGFRB levels can serve as a biomarker for PDGFRB inhibition as a novel targeted therapeutic strategy in their treatment regimen.

Published
2023

15. Description of a novel subtype of acute myeloid leukemia defined by recurrent CBFB insertions.

Author

Ryland, Georgina L, Umeda, Masayuki, Holmfeldt, Linda, Lehmann, Sören, Herlin, Morten Krogh, Ma, Jing, Khanlari, Mahsa, Rubnitz, Jeffrey E, Ries, Rhonda E, Kosasih, Hansen J, Ekert, Paul G, Goh, Hwee Ngee, Tiong, Ing S, Grimmond, Sean M, Haferlach, Claudia, Day, Ryan B, Ley, Timothy J, Meshinchi, Soheil, Ma, Xiaotu, Blombery, Piers, Klco, Jeffery M, Ryland, Georgina L, Umeda, Masayuki, Holmfeldt, Linda, Lehmann, Sören, Herlin, Morten Krogh, Ma, Jing, Khanlari, Mahsa, Rubnitz, Jeffrey E, Ries, Rhonda E, Kosasih, Hansen J, Ekert, Paul G, Goh, Hwee Ngee, Tiong, Ing S, Grimmond, Sean M, Haferlach, Claudia, Day, Ryan B, Ley, Timothy J, Meshinchi, Soheil, Ma, Xiaotu, Blombery, Piers, and Klco, Jeffery M

Published
2023
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16. Description of a novel subtype of acute myeloid leukemia defined by recurrent CBFB insertions

Author

Ryland, Georgina L., primary, Umeda, Masayuki, additional, Holmfeldt, Linda, additional, Lehmann, Sören, additional, Herlin, Morten Krogh, additional, Ma, Jing, additional, Khanlari, Mahsa, additional, Rubnitz, Jeffrey E., additional, Ries, Rhonda E., additional, Kosasih, Hansen J., additional, Ekert, Paul G., additional, Goh, Hwee Ngee, additional, Tiong, Ing S., additional, Grimmond, Sean M., additional, Haferlach, Claudia, additional, Day, Ryan B., additional, Ley, Timothy J., additional, Meshinchi, Soheil, additional, Ma, Xiaotu, additional, Blombery, Piers, additional, and Klco, Jeffery M., additional

Published
2023
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20. ALLSorts: a RNA-Seq classifier for B-Cell Acute Lymphoblastic Leukemia

Author

Schmidt, Breon, primary, Brown, Lauren M., additional, Ryland, Georgina L., additional, Lonsdale, Andrew, additional, Kosasih, Hansen J., additional, Ludlow, Louise E., additional, Majewski, Ian J., additional, Blombery, Piers, additional, Ekert, Paul G., additional, Davidson, Nadia M., additional, and Oshlack, Alicia, additional

Published
2021
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22. Human MLL/KMT2A gene exhibits a second breakpoint cluster region for recurrent MLL–USP2 fusions

Author

Meyer, C, Lopes, B, Caye-Eude, A, Cavé, H, Arfeuille, C, Cuccuini, W, Sutton, R, Venn, N, Oh, S, Tsaur, G, Escherich, G, Feuchtinger, T, Kosasih, H, Khaw, S, Ekert, P, Pombo-de-Oliveira, M, Bidet, A, Djahanschiri, B, Ebersberger, I, Zaliova, M, Zuna, J, Zermanova, Z, Juvonen, V, Grümayer, R, Fazio, G, Cazzaniga, G, Larghero, P, Emerenciano, M, Marschalek, R, Meyer, Claus, Lopes, Bruno A., Caye-Eude, Aurélie, Cavé, Hélène, Arfeuille, Chloé, Cuccuini, Wendy, Sutton, Rosemary, Venn, Nicola C., Oh, Seung Hwan, Tsaur, Grigory, Escherich, Gabriele, Feuchtinger, Tobias, Kosasih, Hansen J., Khaw, Seong L., Ekert, Paul G., Pombo-de-Oliveira, Maria S., Bidet, Audrey, Djahanschiri, Bardya, Ebersberger, Ingo, Zaliova, Marketa, Zuna, Jan, Zermanova, Zuzana, Juvonen, Vesa, Grümayer, Renate Panzer, Fazio, Grazia, Cazzaniga, Gianni, Larghero, Patrizia, Emerenciano, Mariana, Marschalek, Rolf, Meyer, C, Lopes, B, Caye-Eude, A, Cavé, H, Arfeuille, C, Cuccuini, W, Sutton, R, Venn, N, Oh, S, Tsaur, G, Escherich, G, Feuchtinger, T, Kosasih, H, Khaw, S, Ekert, P, Pombo-de-Oliveira, M, Bidet, A, Djahanschiri, B, Ebersberger, I, Zaliova, M, Zuna, J, Zermanova, Z, Juvonen, V, Grümayer, R, Fazio, G, Cazzaniga, G, Larghero, P, Emerenciano, M, Marschalek, R, Meyer, Claus, Lopes, Bruno A., Caye-Eude, Aurélie, Cavé, Hélène, Arfeuille, Chloé, Cuccuini, Wendy, Sutton, Rosemary, Venn, Nicola C., Oh, Seung Hwan, Tsaur, Grigory, Escherich, Gabriele, Feuchtinger, Tobias, Kosasih, Hansen J., Khaw, Seong L., Ekert, Paul G., Pombo-de-Oliveira, Maria S., Bidet, Audrey, Djahanschiri, Bardya, Ebersberger, Ingo, Zaliova, Marketa, Zuna, Jan, Zermanova, Zuzana, Juvonen, Vesa, Grümayer, Renate Panzer, Fazio, Grazia, Cazzaniga, Gianni, Larghero, Patrizia, Emerenciano, Mariana, and Marschalek, Rolf

Published
2019

23. MLL-TFE3: a novel and aggressive KMT2Afusion identified in infant leukemia

Author

Kosasih, Hansen J., Davidson, Nadia M., Bjelosevic, Stefan, Morrish, Emma, Brennan, Margs S., Oshlack, Alicia, Johnstone, Ricky W., Brumatti, Gabriela, Khaw, Seong L., and Ekert, Paul G.

Abstract

•A novel KMT2A-rearrangement, MLL-TFE3, was identified in an infant leukemia patient.•MLL-TFE3 expression produces aggressive leukemia in a mouse model.

Published
2020
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24. Human MLL/KMT2Agene exhibits a second breakpoint cluster region for recurrent MLL–USP2 fusions

Author

Meyer, Claus, Lopes, Bruno A., Caye-Eude, Aurélie, Cavé, Hélène, Arfeuille, Chloé, Cuccuini, Wendy, Sutton, Rosemary, Venn, Nicola C., Oh, Seung Hwan, Tsaur, Grigory, Escherich, Gabriele, Feuchtinger, Tobias, Kosasih, Hansen J., Khaw, Seong L., Ekert, Paul G., Pombo-de-Oliveira, Maria S., Bidet, Audrey, Djahanschiri, Bardya, Ebersberger, Ingo, Zaliova, Marketa, Zuna, Jan, Zermanova, Zuzana, Juvonen, Vesa, Grümayer, Renate Panzer, Fazio, Grazia, Cazzaniga, Gianni, Larghero, Patrizia, Emerenciano, Mariana, and Marschalek, Rolf

Published
2019
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25. Targeting hyperactive platelet-derived growth factor receptor-β signaling in T-cell acute lymphoblastic leukemia and lymphoma.

Author

De Coninck S, De Smedt R, Lintermans B, Reunes L, Kosasih HJ, Reekmans A, Brown LM, Van Roy N, Palhais B, Roels J, Van der Linden M, Van Dorpe J, Ntziachristos P, Van Delft FW, Mansour MR, Pieters T, Lammens T, De Moerloose B, De Bock CE, Goossens S, and Van Vlierberghe P

Subjects
Humans, Animals, Mice, Xenograft Model Antitumor Assays, Cell Line, Tumor, Oncogene Proteins, Fusion genetics, Oncogene Proteins, Fusion metabolism, Myosin Heavy Chains genetics, Myosin Heavy Chains metabolism, Molecular Targeted Therapy, Protein Kinase Inhibitors pharmacology, Protein Kinase Inhibitors therapeutic use, Disease Models, Animal, Receptor, Platelet-Derived Growth Factor beta genetics, Receptor, Platelet-Derived Growth Factor beta metabolism, Receptor, Platelet-Derived Growth Factor beta antagonists & inhibitors, Precursor T-Cell Lymphoblastic Leukemia-Lymphoma drug therapy, Precursor T-Cell Lymphoblastic Leukemia-Lymphoma metabolism, Precursor T-Cell Lymphoblastic Leukemia-Lymphoma genetics, Precursor T-Cell Lymphoblastic Leukemia-Lymphoma pathology, Signal Transduction drug effects
Abstract

T-cell acute lymphoblastic leukemia (T-ALL) and T-cell lymphoblastic lymphoma (T-LBL) are rare aggressive hematologic malignancies. Current treatment consists of intensive chemotherapy leading to 80% overall survival but is associated with severe toxic side effects. Furthermore, 10-20% of patients still die from relapsed or refractory disease providing a strong rationale for more specific, targeted therapeutic strategies with less toxicities. Here, we report a novel MYH9::PDGFRB fusion in a T-LBL patient, and demonstrate that this fusion product is constitutively active and sufficient to drive oncogenic transformation in vitro and in vivo. Expanding our analysis more broadly across T-ALL, we found a T-ALL cell line and multiple patient-derived xenograft models with PDGFRB hyperactivation in the absence of a fusion, with high PDGFRB expression in TLX3 and HOXA T-ALL molecular subtypes. To target this PDGFRB hyperactivation, we evaluated the therapeutic effects of a selective PDGFRB inhibitor, CP-673451, both in vitro and in vivo and demonstrated sensitivity if the receptor is hyperactivated. Altogether, our work reveals that hyperactivation of PDGFRB is an oncogenic driver in T-ALL/T-LBL, and that screening T-ALL/T-LBL patients for phosphorylated PDGFRB levels can serve as a biomarker for PDGFRB inhibition as a novel targeted therapeutic strategy in their treatment regimen.

Published
2024
Full Text
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