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1. Context-restricted PD-(L)1 checkpoint agonism by CTLA4-Ig therapies inhibits T cell activity

Author

Oxley, Ethan P., Kershaw, Nadia J., Louis, Cynthia, Goodall, Katharine J., Garwood, Maximilian M., Jee Ho, Skye Min, Voo, Veronica T.F., Park, Hae-Young, Iaria, Josephine, Wong, Lilian L.L., Lebenbaum, Ariel G., Wiranata, Stephanie, Pang, Ee Shan, Edwards, Emily S.J., D’Silva, Damian B., Hansen, Jacinta, van Zelm, Menno C., O’Keeffe, Meredith, Hogarth, P. Mark, Haynes, Nicole M., Huntington, Nicholas D., Wicks, Ian P., and Dickins, Ross A.

Published
2024
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2. Author Correction: Metabolic gatekeeper function of B-lymphoid transcription factors

Author

Chan, Lai N, Chen, Zhengshan, Braas, Daniel, Lee, Jae-Woong, Xiao, Gang, Geng, Huimin, Cosgun, Kadriye Nehir, Hurtz, Christian, Shojaee, Seyedmehdi, Cazzaniga, Valeria, Schjerven, Hilde, Ernst, Thomas, Hochhaus, Andreas, Kornblau, Steven M, Konopleva, Marina, Pufall, Miles A, Cazzaniga, Giovanni, Liu, Grace J, Milne, Thomas A, Koeffler, H Phillip, Ross, Theodora S, Sánchez-García, Isidro, Borkhardt, Arndt, Yamamoto, Keith R, Dickins, Ross A, Graeber, Thomas G, and Müschen, Markus

Subjects
Information and Computing Sciences, Communications Engineering, Engineering, General Science & Technology
Abstract

In Fig. 3c of this Letter, the the effects of CRISPR-Cas9-mediated deletion of NR3C1, TXNIP and CNR2 in patient-derived B-lineage leukaemia cells were shown. For curves depicting NR3C1 (left graph), data s for TXNIP (middle graph) were inadvertently plotted. This figure has been corrected online, and the original Fig. 3c is shown as Supplementary Information to this Amendment for transparency. The error does not affect the conclusions of the Letter. In addition, Source Data files have been added for the Figs. 1-4 and Extended Data Figs. 1-10 of the original Letter.

Published
2018

3. Metabolic gatekeeper function of B-lymphoid transcription factors.

Author

Chan, Lai N, Chen, Zhengshan, Braas, Daniel, Lee, Jae-Woong, Xiao, Gang, Geng, Huimin, Cosgun, Kadriye Nehir, Hurtz, Christian, Shojaee, Seyedmehdi, Cazzaniga, Valeria, Schjerven, Hilde, Ernst, Thomas, Hochhaus, Andreas, Kornblau, Steven M, Konopleva, Marina, Pufall, Miles A, Cazzaniga, Giovanni, Liu, Grace J, Milne, Thomas A, Koeffler, H Phillip, Ross, Theodora S, Sánchez-García, Isidro, Borkhardt, Arndt, Yamamoto, Keith R, Dickins, Ross A, Graeber, Thomas G, and Müschen, Markus

Subjects
B-Lymphocytes, Animals, Mice, Transgenic, Humans, Mice, Disease Models, Animal, Pyruvic Acid, Protein-Serine-Threonine Kinases, Glucose, Carrier Proteins, Receptor, Cannabinoid, CB2, Receptors, Glucocorticoid, Transcription Factors, Adenosine Triphosphate, Glucocorticoids, Chromatin Immunoprecipitation, Sequence Analysis, RNA, Cell Death, Gene Expression Regulation, Neoplastic, Citric Acid Cycle, Energy Metabolism, Female, Ikaros Transcription Factor, Precursor B-Cell Lymphoblastic Leukemia-Lymphoma, AMP-Activated Protein Kinases, Carcinogenesis, PAX5 Transcription Factor, Transgenic, Disease Models, Animal, Receptor, Cannabinoid, CB2, Receptors, Glucocorticoid, Sequence Analysis, RNA, Gene Expression Regulation, Neoplastic, General Science & Technology
Abstract

B-lymphoid transcription factors, such as PAX5 and IKZF1, are critical for early B-cell development, yet lesions of the genes encoding these transcription factors occur in over 80% of cases of pre-B-cell acute lymphoblastic leukaemia (ALL). The importance of these lesions in ALL has, until now, remained unclear. Here, by combining studies using chromatin immunoprecipitation with sequencing and RNA sequencing, we identify a novel B-lymphoid program for transcriptional repression of glucose and energy supply. Our metabolic analyses revealed that PAX5 and IKZF1 enforce a state of chronic energy deprivation, resulting in constitutive activation of the energy-stress sensor AMPK. Dominant-negative mutants of PAX5 and IKZF1, however, relieved this glucose and energy restriction. In a transgenic pre-B ALL mouse model, the heterozygous deletion of Pax5 increased glucose uptake and ATP levels by more than 25-fold. Reconstitution of PAX5 and IKZF1 in samples from patients with pre-B ALL restored a non-permissive state and induced energy crisis and cell death. A CRISPR/Cas9-based screen of PAX5 and IKZF1 transcriptional targets identified the products of NR3C1 (encoding the glucocorticoid receptor), TXNIP (encoding a glucose-feedback sensor) and CNR2 (encoding a cannabinoid receptor) as central effectors of B-lymphoid restriction of glucose and energy supply. Notably, transport-independent lipophilic methyl-conjugates of pyruvate and tricarboxylic acid cycle metabolites bypassed the gatekeeper function of PAX5 and IKZF1 and readily enabled leukaemic transformation. Conversely, pharmacological TXNIP and CNR2 agonists and a small-molecule AMPK inhibitor strongly synergized with glucocorticoids, identifying TXNIP, CNR2 and AMPK as potential therapeutic targets. Furthermore, our results provide a mechanistic explanation for the empirical finding that glucocorticoids are effective in the treatment of B-lymphoid but not myeloid malignancies. Thus, B-lymphoid transcription factors function as metabolic gatekeepers by limiting the amount of cellular ATP to levels that are insufficient for malignant transformation.

Published
2017

4. T-ALL can evolve to oncogene independence

Author

Abdulla, Hesham, Vo, Anh, Shields, Benjamin J., Davies, Tenae J., Jackson, Jacob T., Alserihi, Raed, Viney, Elizabeth M., Wong, Tin, Yan, Feng, Wong, Nicholas C., Demoen, Lisa, Curtis, David J., Alexander, Warren S., Van Vlierberghe, Pieter, Dickins, Ross A., and McCormack, Matthew P.

Published
2021
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6. Oncogenic cooperation between TCF7-SPI1 and NRAS(G12D) requires β-catenin activity to drive T-cell acute lymphoblastic leukemia

Author

Van Thillo, Quentin, De Bie, Jolien, Seneviratne, Janith A., Demeyer, Sofie, Omari, Sofia, Balachandran, Anushree, Zhai, Vicki, Tam, Wai L., Sweron, Bram, Geerdens, Ellen, Gielen, Olga, Provost, Sarah, Segers, Heidi, Boeckx, Nancy, Marshall, Glenn M., Cheung, Belamy B., Isobe, Kiyotaka, Kato, Itaru, Takita, Junko, Amos, Timothy G., Deveson, Ira W., McCalmont, Hannah, Lock, Richard B., Oxley, Ethan P., Garwood, Maximilian M., Dickins, Ross A., Uyttebroeck, Anne, Carter, Daniel R., Cools, Jan, and de Bock, Charles E.

Published
2021
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7. MLL3 Is a Haploinsufficient 7q Tumor Suppressor in Acute Myeloid Leukemia

Author

Chen, Chong, Liu, Yu, Rappaport, Amy R, Kitzing, Thomas, Schultz, Nikolaus, Zhao, Zhen, Shroff, Aditya S, Dickins, Ross A, Vakoc, Christopher R, Bradner, James E, Stock, Wendy, LeBeau, Michelle M, Shannon, Kevin M, Kogan, Scott, Zuber, Johannes, and Lowe, Scott W

Subjects
Biological Sciences, Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Cancer, Hematology, Childhood Leukemia, Stem Cell Research, Genetics, Pediatric Cancer, Biotechnology, Pediatric, Rare Diseases, Animals, Azepines, Cell Differentiation, Cell Transformation, Neoplastic, Chromosome Deletion, Chromosomes, Human, Pair 7, Clustered Regularly Interspaced Short Palindromic Repeats, Drug Resistance, Neoplasm, Gene Dosage, Haploinsufficiency, Histone-Lysine N-Methyltransferase, Humans, Leukemia, Myeloid, Acute, Mice, Mice, Inbred C57BL, Myeloid-Lymphoid Leukemia Protein, RNA Interference, RNA, Small Interfering, Triazoles, Tumor Suppressor Proteins, Neurosciences, Oncology & Carcinogenesis, Biochemistry and cell biology, Oncology and carcinogenesis
Abstract

Recurring deletions of chromosome 7 and 7q [-7/del(7q)] occur in myelodysplastic syndromes and acute myeloid leukemia (AML) and are associated with poor prognosis. However, the identity of functionally relevant tumor suppressors on 7q remains unclear. Using RNAi and CRISPR/Cas9 approaches, we show that an ∼50% reduction in gene dosage of the mixed lineage leukemia 3 (MLL3) gene, located on 7q36.1, cooperates with other events occurring in -7/del(7q) AMLs to promote leukemogenesis. Mll3 suppression impairs the differentiation of HSPC. Interestingly, Mll3-suppressed leukemias, like human -7/del(7q) AMLs, are refractory to conventional chemotherapy but sensitive to the BET inhibitor JQ1. Thus, our mouse model functionally validates MLL3 as a haploinsufficient 7q tumor suppressor and suggests a therapeutic option for this aggressive disease.

Published
2014

9. Supplementary Methods, Figures 1 - 3, Tables 1 - 3 from Molecular and Biologic Analysis of Histone Deacetylase Inhibitors with Diverse Specificities

Author

Newbold, Andrea, primary, Matthews, Geoffrey M., primary, Bots, Michael, primary, Cluse, Leonie A., primary, Clarke, Christopher J.P., primary, Banks, Kellie-Marie, primary, Cullinane, Carleen, primary, Bolden, Jessica E., primary, Christiansen, Ailsa J., primary, Dickins, Ross A., primary, Miccolo, Claudia, primary, Chiocca, Susanna, primary, Kral, Astrid M., primary, Ozerova, Nicole D., primary, Miller, Thomas A., primary, Methot, Joey L., primary, Richon, Victoria M., primary, Secrist, J. Paul, primary, Minucci, Saverio, primary, and Johnstone, Ricky W., primary

Published
2023
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15. The EMT modulator SNAI1 contributes to AML pathogenesis via its interaction with LSD1

Author

Carmichael, Catherine L., primary, Wang, Jueqiong, additional, Nguyen, Thao, additional, Kolawole, Oluseyi, additional, Benyoucef, Aissa, additional, De Mazière, Charlotte, additional, Milne, Anna R., additional, Samuel, Sona, additional, Gillinder, Kevin, additional, Hediyeh-zadeh, Soroor, additional, Vo, Anh N. Q., additional, Huang, Yizhou, additional, Knezevic, Kathy, additional, McInnes, William R. L., additional, Shields, Benjamin J., additional, Mitchell, Helen, additional, Ritchie, Matthew E., additional, Lammens, Tim, additional, Lintermans, Beatrice, additional, Van Vlierberghe, Pieter, additional, Wong, Nicholas C., additional, Haigh, Katharina, additional, Thoms, Julie A. I., additional, Toulmin, Emma, additional, Curtis, David J., additional, Oxley, Ethan P., additional, Dickins, Ross A., additional, Beck, Dominik, additional, Perkins, Andrew, additional, McCormack, Matthew P., additional, Davis, Melissa J., additional, Berx, Geert, additional, Zuber, Johannes, additional, Pimanda, John E., additional, Kile, Benjamin T., additional, Goossens, Steven, additional, and Haigh, Jody J., additional

Published
2020
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16. 2000 - MONOLINEAGE ORIGIN OF RELAPSE FOLLOWING MULTILINEAGE DIFFERENTIATION THERAPY OF ACUTE MYELOID LEUKEMIA

Author

Dickins, Ross, primary, Ngo, Steven, additional, Oxley, Ethan, additional, Ghisi, Margherita, additional, McKenzie, Mark, additional, Garwood, Maximilian, additional, Jayakrishnan, Swathy, additional, Susanto, Olivia, additional, Mitchell, Helen, additional, Hickey, Michael, additional, Perkins, Andrew, additional, Kile, Benjamin, additional, and Dickins, Ross, additional

Published
2019
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21. Interconversion between Tumorigenic and Differentiated States in Acute Myeloid Leukemia

Author

McKenzie, Mark D., primary, Ghisi, Margherita, additional, Oxley, Ethan P., additional, Ngo, Steven, additional, Cimmino, Luisa, additional, Esnault, Cécile, additional, Liu, Ruijie, additional, Salmon, Jessica M., additional, Bell, Charles C., additional, Ahmed, Nouraiz, additional, Erlichster, Michael, additional, Witkowski, Matthew T., additional, Liu, Grace J., additional, Chopin, Michael, additional, Dakic, Aleksandar, additional, Simankowicz, Emilia, additional, Pomilio, Giovanna, additional, Vu, Tina, additional, Krsmanovic, Pavle, additional, Su, Shian, additional, Tian, Luyi, additional, Baldwin, Tracey M., additional, Zalcenstein, Daniela A., additional, DiRago, Ladina, additional, Wang, Shu, additional, Metcalf, Donald, additional, Johnstone, Ricky W., additional, Croker, Ben A., additional, Lancaster, Graeme I., additional, Murphy, Andrew J., additional, Naik, Shalin H., additional, Nutt, Stephen L., additional, Pospisil, Vitek, additional, Schroeder, Timm, additional, Wall, Meaghan, additional, Dawson, Mark A., additional, Wei, Andrew H., additional, de Thé, Hugues, additional, Ritchie, Matthew E., additional, Zuber, Johannes, additional, and Dickins, Ross A., additional

Published
2019
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23. Transcription Factor PU.1 Promotes Conventional Dendritic Cell Identity and Function via Induction of Transcriptional Regulator DC-SCRIPT

Author

Chopin, Michaël, primary, Lun, Aaron T., additional, Zhan, Yifan, additional, Schreuder, Jaring, additional, Coughlan, Hannah, additional, D’Amico, Angela, additional, Mielke, Lisa A., additional, Almeida, Francisca F., additional, Kueh, Andrew J., additional, Dickins, Ross A., additional, Belz, Gabrielle T., additional, Naik, Shalin H., additional, Lew, Andrew M., additional, Bouillet, Phillipe, additional, Herold, Marco J., additional, Smyth, Gordon K., additional, Corcoran, Lynn M., additional, and Nutt, Stephen L., additional

Published
2019
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24. Generation of an inducible mouse model to reversibly silence Stat3

Author

Alorro, Mariah, Pierce, Thomas, Eissmann, Moritz, Dijkstra, Christine, Dickins, Ross, Ernst, Matthias, Buchert, Michael, Masson, Frédéric, Institut de Génomique Fonctionnelle (IGF), Université de Montpellier (UM)-Université Montpellier 1 (UM1)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Montpellier 2 - Sciences et Techniques (UM2)-Centre National de la Recherche Scientifique (CNRS), Institut de physique du globe de Strasbourg (IPGS), and Université de Strasbourg (UNISTRA)-Institut national des sciences de l'Univers (INSU - CNRS)-Centre National de la Recherche Scientifique (CNRS)

Subjects
[SDV]Life Sciences [q-bio], ComputingMilieux_MISCELLANEOUS
Abstract

International audience

Published
2017
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26. Metabolic gatekeeper function of B-lymphoid transcription factors

Author

Chan, L, Chen, Z, Braas, D, Lee, J, Xiao, G, Geng, H, Cosgun, K, Hurtz, C, Shojaee, S, Cazzaniga, V, Schjerven, H, Ernst, T, Hochhaus, A, Kornblau, S, Konopleva, M, Pufall, M, Cazzaniga, G, Liu, G, Milne, T, Koeffler, H, Ross, T, Sánchez-García, I, Borkhardt, A, Yamamoto, K, Dickins, R, Graeber, T, Müschen, M, Chan, Lai N., Chen, Zhengshan, Braas, Daniel, Lee, Jae-Woong, Xiao, Gang, Geng, Huimin, Cosgun, Kadriye Nehir, Hurtz, Christian, Shojaee, Seyedmehdi, Cazzaniga, Valeria, Schjerven, Hilde, Ernst, Thomas, Hochhaus, Andreas, Kornblau, Steven M., Konopleva, Marina, Pufall, Miles A., Cazzaniga, Giovanni, Liu, Grace J., Milne, Thomas A., Koeffler, H. Phillip, Ross, Theodora S., Sánchez-García, Isidro, Borkhardt, Arndt, Yamamoto, Keith R., Dickins, Ross A., Graeber, Thomas G., Müschen, Markus, Chan, L, Chen, Z, Braas, D, Lee, J, Xiao, G, Geng, H, Cosgun, K, Hurtz, C, Shojaee, S, Cazzaniga, V, Schjerven, H, Ernst, T, Hochhaus, A, Kornblau, S, Konopleva, M, Pufall, M, Cazzaniga, G, Liu, G, Milne, T, Koeffler, H, Ross, T, Sánchez-García, I, Borkhardt, A, Yamamoto, K, Dickins, R, Graeber, T, Müschen, M, Chan, Lai N., Chen, Zhengshan, Braas, Daniel, Lee, Jae-Woong, Xiao, Gang, Geng, Huimin, Cosgun, Kadriye Nehir, Hurtz, Christian, Shojaee, Seyedmehdi, Cazzaniga, Valeria, Schjerven, Hilde, Ernst, Thomas, Hochhaus, Andreas, Kornblau, Steven M., Konopleva, Marina, Pufall, Miles A., Cazzaniga, Giovanni, Liu, Grace J., Milne, Thomas A., Koeffler, H. Phillip, Ross, Theodora S., Sánchez-García, Isidro, Borkhardt, Arndt, Yamamoto, Keith R., Dickins, Ross A., Graeber, Thomas G., and Müschen, Markus

Abstract

B-lymphoid transcription factors, such as PAX5 and IKZF1, are critical for early B-cell development, yet lesions of the genes encoding these transcription factors occur in over 80% of cases of pre-B-cell acute lymphoblastic leukaemia (ALL). The importance of these lesions in ALL has, until now, remained unclear. Here, by combining studies using chromatin immunoprecipitation with sequencing and RNA sequencing, we identify a novel B-lymphoid program for transcriptional repression of glucose and energy supply. Our metabolic analyses revealed that PAX5 and IKZF1 enforce a state of chronic energy deprivation, resulting in constitutive activation of the energy-stress sensor AMPK. Dominant-negative mutants of PAX5 and IKZF1, however, relieved this glucose and energy restriction. In a transgenic pre-B ALL mouse model, the heterozygous deletion of Pax5 increased glucose uptake and ATP levels by more than 25-fold. Reconstitution of PAX5 and IKZF1 in samples from patients with pre-B ALL restored a non-permissive state and induced energy crisis and cell death. A CRISPR/Cas9-based screen of PAX5 and IKZF1 transcriptional targets identified the products of NR3C1 (encoding the glucocorticoid receptor), TXNIP (encoding a glucose-feedback sensor) and CNR2 (encoding a cannabinoid receptor) as central effectors of B-lymphoid restriction of glucose and energy supply. Notably, transport-independent lipophilic methyl-conjugates of pyruvate and tricarboxylic acid cycle metabolites bypassed the gatekeeper function of PAX5 and IKZF1 and readily enabled leukaemic transformation. Conversely, pharmacological TXNIP and CNR2 agonists and a small-molecule AMPK inhibitor strongly synergized with glucocorticoids, identifying TXNIP, CNR2 and AMPK as potential therapeutic targets. Furthermore, our results provide a mechanistic explanation for the empirical finding that glucocorticoids are effective in the treatment of B-lymphoid but not myeloid malignancies. Thus, B-lymphoid transcription factors fun

Published
2017

27. Metabolic gatekeeper function of B-lymphoid transcription factors

Author

Wellcome Trust, Melanoma Research Alliance (US), Howard Hughes Medical Institute, Josep Carreras Leukemia Foundation, American Cancer Society, National Institutes of Health (US), Federal Ministry of Education and Research (Germany), Chan, Lai N., Chen, Zhengshan, Braas, Daniel, Lee, Jae-Woong, Xiao, Gang, Huimin, Geng, Cosgun, Kadriye Nehir, Hurtz, Christian, Shojaee, Seyedmehdi, Cazzaniga, Valeria, Schjerven, Hilde, Ernst, Thomas, Hochhaus, Andreas, Kornblau, Steven M., Konopleva, Marina, Pufall, Miles A., Cazzaniga, Giovanni, Liu, Grace J., Milne, Thomas A., Koeffler, H. Philip, Ross, Theodora S., Sánchez García, Isidro, Borkhardt, Arndt, Yamamoto, Keith R., Dickins, Ross A., Graeber, Thomas G., Müschen, Markus, Wellcome Trust, Melanoma Research Alliance (US), Howard Hughes Medical Institute, Josep Carreras Leukemia Foundation, American Cancer Society, National Institutes of Health (US), Federal Ministry of Education and Research (Germany), Chan, Lai N., Chen, Zhengshan, Braas, Daniel, Lee, Jae-Woong, Xiao, Gang, Huimin, Geng, Cosgun, Kadriye Nehir, Hurtz, Christian, Shojaee, Seyedmehdi, Cazzaniga, Valeria, Schjerven, Hilde, Ernst, Thomas, Hochhaus, Andreas, Kornblau, Steven M., Konopleva, Marina, Pufall, Miles A., Cazzaniga, Giovanni, Liu, Grace J., Milne, Thomas A., Koeffler, H. Philip, Ross, Theodora S., Sánchez García, Isidro, Borkhardt, Arndt, Yamamoto, Keith R., Dickins, Ross A., Graeber, Thomas G., and Müschen, Markus

Abstract

B-lymphoid transcription factors, such as PAX5 and IKZF1, are critical for early B-cell development, yet lesions of the genes encoding these transcription factors occur in over 80% of cases of pre-B-cell acute lymphoblastic leukaemia (ALL). The importance of these lesions in ALL has, until now, remained unclear. Here, by combining studies using chromatin immunoprecipitation with sequencing and RNA sequencing, we identify a novel B-lymphoid program for transcriptional repression of glucose and energy supply. Our metabolic analyses revealed that PAX5 and IKZF1 enforce a state of chronic energy deprivation, resulting in constitutive activation of the energy-stress sensor AMPK. Dominant-negative mutants of PAX5 and IKZF1, however, relieved this glucose and energy restriction. In a transgenic pre-B ALL mouse model, the heterozygous deletion of Pax5 increased glucose uptake and ATP levels by more than 25-fold. Reconstitution of PAX5 and IKZF1 in samples from patients with pre-B ALL restored a non-permissive state and induced energy crisis and cell death. A CRISPR/Cas9-based screen of PAX5 and IKZF1 transcriptional targets identified the products of NR3C1 (encoding the glucocorticoid receptor), TXNIP (encoding a glucose-feedback sensor) and CNR2 (encoding a cannabinoid receptor) as central effectors of B-lymphoid restriction of glucose and energy supply. Notably, transport-independent lipophilic methyl-conjugates of pyruvate and tricarboxylic acid cycle metabolites bypassed the gatekeeper function of PAX5 and IKZF1 and readily enabled leukaemic transformation. Conversely, pharmacological TXNIP and CNR2 agonists and a small-molecule AMPK inhibitor strongly synergized with glucocorticoids, identifying TXNIP, CNR2 and AMPK as potential therapeutic targets. Furthermore, our results provide a mechanistic explanation for the empirical finding that glucocorticoids are effective in the treatment of B-lymphoid but not myeloid malignancies. Thus, B-lymphoid transcription factors fun

Published
2017

28. Restoration of TET2 Function Blocks Aberrant Self-Renewal and Leukemia Progression

Author

Cimmino, Luisa, primary, Dolgalev, Igor, additional, Wang, Yubao, additional, Yoshimi, Akihide, additional, Martin, Gaëlle H., additional, Wang, Jingjing, additional, Ng, Victor, additional, Xia, Bo, additional, Witkowski, Matthew T., additional, Mitchell-Flack, Marisa, additional, Grillo, Isabella, additional, Bakogianni, Sofia, additional, Ndiaye-Lobry, Delphine, additional, Martín, Miguel Torres, additional, Guillamot, Maria, additional, Banh, Robert S., additional, Xu, Mingjiang, additional, Figueroa, Maria E., additional, Dickins, Ross A., additional, Abdel-Wahab, Omar, additional, Park, Christopher Y., additional, Tsirigos, Aristotelis, additional, Neel, Benjamin G., additional, and Aifantis, Iannis, additional

Published
2017
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30. Genomic characterisation of Eμ-Myc mouse lymphomas identifies Bcor as a Myc co-operative tumour-suppressor gene

Author

Lefebure, Marcus, primary, Tothill, Richard W., additional, Kruse, Elizabeth, additional, Hawkins, Edwin D., additional, Shortt, Jake, additional, Matthews, Geoffrey M., additional, Gregory, Gareth P., additional, Martin, Benjamin P., additional, Kelly, Madison J., additional, Todorovski, Izabela, additional, Doyle, Maria A., additional, Lupat, Richard, additional, Li, Jason, additional, Schroeder, Jan, additional, Wall, Meaghan, additional, Craig, Stuart, additional, Poortinga, Gretchen, additional, Cameron, Don, additional, Bywater, Megan, additional, Kats, Lev, additional, Gearhart, Micah D., additional, Bardwell, Vivian J., additional, Dickins, Ross A., additional, Hannan, Ross D., additional, Papenfuss, Anthony T., additional, and Johnstone, Ricky W., additional

Published
2017
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31. Conserved IKAROS-regulated genes associated with B-progenitor acute lymphoblastic leukemia outcome

Author

Witkowski, Matthew T., primary, Hu, Yifang, additional, Roberts, Kathryn G., additional, Boer, Judith M., additional, McKenzie, Mark D., additional, Liu, Grace J., additional, Le Grice, Oliver D., additional, Tremblay, Cedric S., additional, Ghisi, Margherita, additional, Willson, Tracy A., additional, Horstmann, Martin A., additional, Aifantis, Iannis, additional, Cimmino, Luisa, additional, Frietze, Seth, additional, den Boer, Monique L., additional, Mullighan, Charles G., additional, Smyth, Gordon K., additional, and Dickins, Ross A., additional

Published
2017
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33. The Transcription Factor PU.1 Controls a Reversible Differentiation Program in Acute Myeloid Leukemia

Author

McKenzie, Mark D, primary, Ghisi, Margherita, additional, Cimmino, Luisa, additional, Erlichster, Michael, additional, Oxley, Ethan P, additional, Liu, Cynthia, additional, Witkowski, Matthew T, additional, Liu, Grace, additional, Dakic, Aleksandar, additional, Simankowicz, Emilia, additional, DiRago, Ladina, additional, Metcalf, Donald, additional, Nutt, Stephen L, additional, Wall, Meaghan, additional, Ritchie, Matthew E, additional, Zuber, Johannes, additional, and Dickins, Ross A, additional

Published
2016
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36. Id2 and E Proteins Orchestrate the Initiation and Maintenance of MLL-Rearranged Acute Myeloid Leukemia

Author

Ghisi, Margherita, primary, Kats, Lev, additional, Masson, Frederick, additional, Li, Jason, additional, Kratina, Tobias, additional, Vidacs, Eva, additional, Gilan, Omer, additional, Doyle, Maria A., additional, Newbold, Andrea, additional, Bolden, Jessica E., additional, Fairfax, Kirsten A., additional, de Graaf, Carolyn A., additional, Firth, Matthew, additional, Zuber, Johannes, additional, Dickins, Ross A., additional, Corcoran, Lynn M., additional, Dawson, Mark A., additional, Belz, Gabrielle T., additional, and Johnstone, Ricky W., additional

Published
2016
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38. B-Lymphoid Transcription Factors Restrict Glycolytic Energy Supply for Oncogenic Signaling

Author

Chan, Lai N, primary, Chen, Zhengshan, additional, Braas, Daniel, additional, Geng, Huimin, additional, Hurtz, Christian, additional, Shojaee, Seyedmehdi, additional, Cazzaniga, Valeria, additional, Ng, Carina, additional, Ernst, Thomas, additional, Hochhaus, Andreas, additional, Kornblau, Steven M, additional, Cazzaniga, Giovanni, additional, Liu, Grace, additional, Milne, Thomas, additional, Koeffler, H. Phillip, additional, Armstrong, Scott A., additional, Dickins, Ross Alexander, additional, Yamamoto, Keith R, additional, Graeber, Thomas G, additional, and Muschen, Markus, additional

Published
2015
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39. Efficacy of Retinoids in IKZF1-Mutated BCR-ABL1 Acute Lymphoblastic Leukemia

Author

Churchman, Michelle L., primary, Low, Jonathan, additional, Qu, Chunxu, additional, Paietta, Elisabeth M., additional, Kasper, Lawryn H., additional, Chang, Yunchao, additional, Payne-Turner, Debbie, additional, Althoff, Mark J., additional, Song, Guangchun, additional, Chen, Shann-Ching, additional, Ma, Jing, additional, Rusch, Michael, additional, McGoldrick, Dan, additional, Edmonson, Michael, additional, Gupta, Pankaj, additional, Wang, Yong-Dong, additional, Caufield, William, additional, Freeman, Burgess, additional, Li, Lie, additional, Panetta, John C., additional, Baker, Sharyn, additional, Yang, Yung-Li, additional, Roberts, Kathryn G., additional, McCastlain, Kelly, additional, Iacobucci, Ilaria, additional, Peters, Jennifer L., additional, Centonze, Victoria E., additional, Notta, Faiyaz, additional, Dobson, Stephanie M., additional, Zandi, Sasan, additional, Dick, John E., additional, Janke, Laura, additional, Peng, Junmin, additional, Kodali, Kiran, additional, Pagala, Vishwajeeth, additional, Min, Jaeki, additional, Mayasundari, Anand, additional, Williams, Richard T., additional, Willman, Cheryl L., additional, Rowe, Jacob, additional, Luger, Selina, additional, Dickins, Ross A., additional, Guy, R. Kiplin, additional, Chen, Taosheng, additional, and Mullighan, Charles G., additional

Published
2015
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41. The class II PI 3-kinase, PI3KC2α, links platelet internal membrane structure to shear-dependent adhesive function

Author

Mountford, Jessica K., primary, Petitjean, Claire, additional, Putra, Harun W. Kusuma, additional, McCafferty, Jonathan A., additional, Setiabakti, Natasha M., additional, Lee, Hannah, additional, Tønnesen, Lotte L., additional, McFadyen, James D., additional, Schoenwaelder, Simone M., additional, Eckly, Anita, additional, Gachet, Christian, additional, Ellis, Sarah, additional, Voss, Anne K., additional, Dickins, Ross A., additional, Hamilton, Justin R., additional, and Jackson, Shaun P., additional

Published
2015
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45. PAX5 loss imposes a reversible differentiation block in b-progenitor acute lymphoblastic leukemia

Author

Liu, Grace, primary, Cimmino, Luisa, additional, Jude, Julian, additional, Hu, Yifang, additional, Kartal, Mutlu, additional, Witkowski, Matthew, additional, McKenzie, Mark, additional, Best, Sarah, additional, Tuohey, Laura, additional, Mullighan, Charles, additional, Farrar, Michael, additional, Nutt, Stephen, additional, Smyth, Gordon, additional, Zuber, Johannes, additional, and Dickins, Ross, additional

Published
2014
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46. Probing IKAROS functions in B-ALL using novel mouse models

Author

Witkowski, Matthew, primary, Hu, Yifang, additional, Sathe, Priyanka, additional, McKenzie, Mark, additional, Cimmino, Luisa, additional, Liu, Grace, additional, Keniry, Andrew, additional, Smyth, Gordon K., additional, Huntington, Nicholas, additional, and Dickins, Ross, additional

Published
2014
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47. Pax5 loss imposes a reversible differentiation block in B-progenitor acute lymphoblastic leukemia

Author

Liu, Grace J., primary, Cimmino, Luisa, additional, Jude, Julian G., additional, Hu, Yifang, additional, Witkowski, Matthew T., additional, McKenzie, Mark D., additional, Kartal-Kaess, Mutlu, additional, Best, Sarah A., additional, Tuohey, Laura, additional, Liao, Yang, additional, Shi, Wei, additional, Mullighan, Charles G., additional, Farrar, Michael A., additional, Nutt, Stephen L., additional, Smyth, Gordon K., additional, Zuber, Johannes, additional, and Dickins, Ross A., additional

Published
2014
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48. shRNA-seq data analysis with edgeR

Author

Dai, Zhiyin, primary, Sheridan, Julie M., additional, Gearing, Linden J., additional, Moore, Darcy L., additional, Su, Shian, additional, Dickins, Ross A., additional, Blewitt, Marnie E., additional, and Ritchie, Matthew E., additional

Published
2014
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50. Molecular and Biologic Analysis of Histone Deacetylase Inhibitors with Diverse Specificities

Author

Newbold, Andrea, primary, Matthews, Geoffrey M., additional, Bots, Michael, additional, Cluse, Leonie A., additional, Clarke, Christopher J.P., additional, Banks, Kellie-Marie, additional, Cullinane, Carleen, additional, Bolden, Jessica E., additional, Christiansen, Ailsa J., additional, Dickins, Ross A., additional, Miccolo, Claudia, additional, Chiocca, Susanna, additional, Kral, Astrid M., additional, Ozerova, Nicole D., additional, Miller, Thomas A., additional, Methot, Joey L., additional, Richon, Victoria M., additional, Secrist, J. Paul, additional, Minucci, Saverio, additional, and Johnstone, Ricky W., additional

Published
2013
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