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12 results on '"Chin, Paulynn S."'

4. 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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5. 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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7. 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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8. 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

11. A FOXO1-induced oncogenic network defines the AML1-ETO preleukemic program.

Author

Shan Lin, Ptasinska, Anetta, Xiaoting Chen, Shrestha, Mahesh, Assi, Salam A., Chin, Paulynn S., Imperato, Maria R., Aronow, B. J., Jingsong Zhang, Weirauch, Matthew T., Bonifer, Constanze, and Mulloy, James C.

Subjects
*PRELEUKEMIA, *STEM cells, *ACUTE myeloid leukemia, *DISEASE relapse, *TUMOR suppressor genes, *DNA-binding proteins, *CANCER cell proliferation, *PREVENTION
Abstract

Understanding and blocking the self-renewal pathway of preleukemia stem cells could prevent acute myeloid leukemia (AML) relapse. In this study, we show that increased FOXO1 represents a critical mechanism driving aberrant self-renewal in preleukemic cells expressing the t(8;21)-associated oncogene AML1-ETO (AE). Although generally considered as a tumor suppressor, FOXO1 is consistently upregulated in t(8;21) AML. Expression of FOXO1in human CD341 cells promotes a preleukemic state with enhanced self-renewal and dysregulated differentiation. The DNA binding domain of FOXO1 is essential for these functions. FOXO1 activates a stem cell molecular signature that is also present in AE preleukemia cells and preserved in t(8;21) patient samples. Genomewide binding studies show that AE and FOXO1 share the majority of their binding sites, whereby FOXO1 binds to multiple crucial self-renewal genes and is required for their activation. In agreement with this observation, genetic and pharmacological ablation of FOXO1 inhibited the long-term proliferation and clonogenicity of AE cells and t(8;21) AML cell lines. Targeting of FOXO1 therefore provides a potential therapeutic strategy for elimination of stem cells at both preleukemic and leukemic stages. [ABSTRACT FROM AUTHOR]

Published
2017
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12. 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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