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Your search keyword '"Kellaway, Sophie G."' showing total 18 results
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18 results on '"Kellaway, Sophie G."'

5. Epigenetic regulator genes direct lineage switching in MLL/AF4 leukemia

Author

Tirtakusuma, Ricky, Szoltysek, Katarzyna, Milne, Paul, Grinev, Vasily V., Ptasinska, Anetta, Chin, Paulynn S., Meyer, Claus, Nakjang, Sirintra, Hehir-Kwa, Jayne Y., Williamson, Daniel, Cauchy, Pierre, Keane, Peter, Assi, Salam A., Ashtiani, Minoo, Kellaway, Sophie G., Imperato, Maria R., Vogiatzi, Fotini, Schweighart, Elizabeth K., Lin, Shan, Wunderlich, Mark, Stutterheim, Janine, Komkov, Alexander, Zerkalenkova, Elena, Evans, Paul, McNeill, Hesta, Elder, Alex, Martinez-Soria, Natalia, Fordham, Sarah E., Shi, Yuzhe, Russell, Lisa J., Pal, Deepali, Smith, Alex, Kingsbury, Zoya, Becq, Jennifer, Eckert, Cornelia, Haas, Oskar A., Carey, Peter, Bailey, Simon, Skinner, Roderick, Miakova, Natalia, Collin, Matthew, Bigley, Venetia, Haniffa, Muzlifah, Marschalek, Rolf, Harrison, Christine J., Cargo, Catherine A., Schewe, Denis, Olshanskaya, Yulia, Thirman, Michael J., Cockerill, Peter N., Mulloy, James C., Blair, Helen J., Vormoor, Josef, Allan, James M., Bonifer, Constanze, Heidenreich, Olaf, and Bomken, Simon

Published
2022
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7. PLCG1 is required for AML1-ETO leukemia stem cell self-renewal

Author

Schnoeder, Tina M., Schwarzer, Adrian, Jayavelu, Ashok Kumar, Hsu, Chen-Jen, Kirkpatrick, Joanna, Döhner, Konstanze, Perner, Florian, Eifert, Theresa, Huber, Nicolas, Arreba-Tutusaus, Patricia, Dolnik, Anna, Assi, Salam A., Nafria, Monica, Jiang, Lu, Dai, Yu-Ting, Chen, Zhu, Chen, Sai-Juan, Kellaway, Sophie G., Ptasinska, Anetta, Ng, Elizabeth S., Stanley, Edouard G., Elefanty, Andrew G., Buschbeck, Marcus, Bierhoff, Holger, Brodt, Steffen, Matziolis, Georg, Fischer, Klaus-Dieter, Hochhaus, Andreas, Chen, Chun-Wei, Heidenreich, Olaf, Mann, Matthias, Lane, Steven W., Bullinger, Lars, Ori, Alessandro, von Eyss, Björn, Bonifer, Constanze, and Heidel, Florian H.

Published
2022
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8. Gene regulatory network analysis predicts cooperating transcription factor regulons required for FLT3-ITD+ AML growth

Author

Coleman, Daniel J L, primary, Keane, Peter, additional, Luque-Martin, Rosario, additional, Chin, Paulynn S, additional, Blair, Helen, additional, Ames, Luke, additional, Kellaway, Sophie G, additional, Griffin, James, additional, Holmes, Elizabeth, additional, Potluri, Sandeep, additional, Assi, Salam A, additional, Bushweller, John H, additional, Heidenreich, Olaf T, additional, Cockerill, Peter, additional, and Bonifer, Constanze, additional

Published
2023
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9. Leukemic stem cells hijack lineage inappropriate signalling pathways to promote their growth

Author

Kellaway, Sophie G, primary, Potluri, Sandeep, additional, Keane, Peter, additional, Blair, Helen, additional, Chin, Paulynn S, additional, Ptasinska, Anetta, additional, Worker, Alice, additional, Ames, Luke, additional, Adamo, Assunta, additional, Coleman, Daniel JL, additional, Khan, Naeem, additional, Assi, Salam, additional, Krippner-Heidenreich, Anja, additional, Raghavan, Manoj, additional, Cockerill, Peter N, additional, Heidenreich, Olaf, additional, and Bonifer, Constanze, additional

Published
2023
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10. Identification and interrogation of the gene regulatory network of CEBPA-double mutant acute myeloid leukemia

Author

Adamo, Assunta, primary, Chin, Paulynn, additional, Keane, Peter, additional, Assi, Salam A., additional, Potluri, Sandeep, additional, Kellaway, Sophie G., additional, Coleman, Daniel, additional, Ames, Luke, additional, Ptasinska, Anetta, additional, Delwel, H. Ruud, additional, Cockerill, Peter N., additional, and Bonifer, Constanze, additional

Published
2022
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11. Epigenetic regulator genes direct lineage switching in MLL/AF4 leukemia

Author

Onderzoek Beeld, Cancer, Tirtakusuma, Ricky, Szoltysek, Katarzyna, Milne, Paul, Grinev, Vasily V, Ptasinska, Anetta, Chin, Paulynn S, Meyer, Claus, Nakjang, Sirintra, Hehir-Kwa, Jayne Y, Williamson, Daniel, Cauchy, Pierre, Keane, Peter, Assi, Salam A, Ashtiani, Minoo, Kellaway, Sophie G, Imperato, Maria R, Vogiatzi, Fotini, Schweighart, Elizabeth K, Lin, Shan, Wunderlich, Mark, Stutterheim, Janine, Komkov, Alexander, Zerkalenkova, Elena, Evans, Paul, McNeill, Hesta, Elder, Alex, Martinez-Soria, Natalia, Fordham, Sarah E, Shi, Yuzhe, Russell, Lisa J, Pal, Deepali, Smith, Alex, Kingsbury, Zoya, Becq, Jennifer, Eckert, Cornelia, Haas, Oskar A, Carey, Peter, Bailey, Simon, Skinner, Roderick, Miakova, Natalia, Collin, Matthew, Bigley, Venetia, Haniffa, Muzlifah, Marschalek, Rolf, Harrison, Christine J, Cargo, Catherine A, Schewe, Denis, Olshanskaya, Yulia, Thirman, Michael J, Cockerill, Peter N, Mulloy, James C, Blair, Helen J, Vormoor, Josef, Allan, James M, Bonifer, Constanze, Heidenreich, Olaf, Bomken, Simon, Onderzoek Beeld, Cancer, Tirtakusuma, Ricky, Szoltysek, Katarzyna, Milne, Paul, Grinev, Vasily V, Ptasinska, Anetta, Chin, Paulynn S, Meyer, Claus, Nakjang, Sirintra, Hehir-Kwa, Jayne Y, Williamson, Daniel, Cauchy, Pierre, Keane, Peter, Assi, Salam A, Ashtiani, Minoo, Kellaway, Sophie G, Imperato, Maria R, Vogiatzi, Fotini, Schweighart, Elizabeth K, Lin, Shan, Wunderlich, Mark, Stutterheim, Janine, Komkov, Alexander, Zerkalenkova, Elena, Evans, Paul, McNeill, Hesta, Elder, Alex, Martinez-Soria, Natalia, Fordham, Sarah E, Shi, Yuzhe, Russell, Lisa J, Pal, Deepali, Smith, Alex, Kingsbury, Zoya, Becq, Jennifer, Eckert, Cornelia, Haas, Oskar A, Carey, Peter, Bailey, Simon, Skinner, Roderick, Miakova, Natalia, Collin, Matthew, Bigley, Venetia, Haniffa, Muzlifah, Marschalek, Rolf, Harrison, Christine J, Cargo, Catherine A, Schewe, Denis, Olshanskaya, Yulia, Thirman, Michael J, Cockerill, Peter N, Mulloy, James C, Blair, Helen J, Vormoor, Josef, Allan, James M, Bonifer, Constanze, Heidenreich, Olaf, and Bomken, Simon

Published
2022

12. A genome-wide relay of signalling-responsive enhancers drives hematopoietic specification

Author

Edginton-White, Benjamin, primary, Maytum, Alexander, additional, Kellaway, Sophie G, additional, Goode, Debbie K, additional, Keane, Peter, additional, Pagnuco, Inti, additional, Assi, Salam A, additional, Ames, Luke, additional, Clarke, Mary L, additional, Cockerill, Peter N, additional, Gottgens, Berthold, additional, Cazier, Jean-Baptiste, additional, and Bonifer, Constanze, additional

Published
2022
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17. Gene regulatory network analysis predicts cooperating transcription factor regulons required for FLT3-ITD+ AML growth.

Author

Coleman DJL, Keane P, Luque-Martin R, Chin PS, Blair H, Ames L, Kellaway SG, Griffin J, Holmes E, Potluri S, Assi SA, Bushweller J, Heidenreich O, Cockerill PN, and Bonifer C

Abstract

AML is a heterogenous disease caused by different mutations. We have previously shown that each mutational sub-type develops its specific gene regulatory network (GRN) with transcription factors interacting with multiple gene modules, many of which are transcription factor genes themselves. Here we hypothesized that highly connected nodes within such networks comprise crucial regulators of AML maintenance. We tested this hypothesis using FLT3-ITD mutated AML as a model and conducted an shRNA drop-out screen informed by this analysis. We show that AML-specific GRNs predict identifying crucial regulatory modules required for AML but not normal cellular growth. Furthermore, our work shows that all modules are highly connected and regulate each other. The careful multi-omic analysis of the role of one (RUNX1) module by shRNA and chemical inhibition shows that this transcription factor and its target genes stabilize the GRN of FLT3-ITD AML and that its removal leads to GRN collapse and cell death., Competing Interests: Conflict of Interest The authors declare no conflict of interest.

Published
2023
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18. RUNX1-EVI1 disrupts lineage determination and the cell cycle by interfering with RUNX1 and EVI1 driven gene regulatory networks.

Author

Kellaway SG, Keane P, Kennett E, and Bonifer C

Subjects
Cell Cycle genetics, Gene Regulatory Networks, Humans, MDS1 and EVI1 Complex Locus Protein genetics, Translocation, Genetic, Core Binding Factor Alpha 2 Subunit genetics, Leukemia, Myeloid, Acute genetics
Abstract

Hematological malignancies are characterised by a block in differentiation, which in many cases is caused by recurrent mutations affecting the activity of hematopoietic transcription factors. RUNX1-EVI1 is a fusion protein formed by the t(3;21) translocation linking two transcription factors required for normal hematopoiesis. RUNX1-EVI1 expression is found in myelodysplastic syndrome, secondary acute myeloid leukemia, and blast crisis of chronic myeloid leukemia; with clinical outcomes being worse than in patients with RUNX1-ETO, RUNX1 or EVI1 mutations alone. RUNX1-EVI1 is usually found as a secondary mutation, therefore the molecular mechanisms underlying how RUNX1-EVI1 alone contributes to poor prognosis are unknown. To address this question, we induced expression of RUNX1-EVI1 in hematopoietic cells derived from an embryonic stem cell differentiation model. Induction resulted in disruption of the RUNX1-dependent endothelial-hematopoietic transition, blocked the cell cycle and undermined cell fate decisions in multipotent hematopoietic progenitor cells. Integrative analyses of gene expression with chromatin and transcription factor binding data demonstrated that RUNX1-EVI1 binding caused the re-distribution of endogenous RUNX1 within the genome and interfered with both RUNX1 and EVI1 regulated gene expression programs. In summary, RUNX1-EVI1 expression alone leads to extensive epigenetic reprogramming which is incompatible with healthy blood production.

Published
2021
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