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28 results on '"Yu, Vionnie W.C."'

1. CRISPR-Cas9 Editing of the HBG1 and HBG2 Promoters to Treat Sickle Cell Disease

Author

Sharma, Akshay, primary, Boelens, Jaap-Jan, additional, Cancio, Maria, additional, Hankins, Jane S., additional, Bhad, Prafulla, additional, Azizy, Marjohn, additional, Lewandowski, Andrew, additional, Zhao, Xiaojun, additional, Chitnis, Shripad, additional, Peddinti, Radhika, additional, Zheng, Yan, additional, Kapoor, Neena, additional, Ciceri, Fabio, additional, Maclachlan, Timothy, additional, Yang, Yi, additional, Liu, Yi, additional, Yuan, Jianping, additional, Naumann, Ulrike, additional, Yu, Vionnie W.C., additional, Stevenson, Susan C., additional, De Vita, Serena, additional, and LaBelle, James L., additional

Published
2023
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2. Inhibiting stromal cell heparan sulfate synthesis improves stem cell mobilization and enables engraftment without cytotoxic conditioning

Author

Saez, Borja, Ferraro, Francesca, Yusuf, Rushdia Z., Cook, Colleen M., Yu, Vionnie W.C., Pardo-Saganta, Ana, Sykes, Stephen M., Palchaudhuri, Rahul, Schajnovitz, Amir, Lotinun, Sutada, Lymperi, Stefania, Mendez-Ferrer, Simon, Toro, Raquel del, Day, Robyn, Vasic, Radovan, Acharya, Sanket S., Baron, Roland, Lin, Charles P., Yamaguchi, Yu, Wagers, Amy J., and Scadden, David T.

Published
2014
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3. Aldehyde dehydrogenase 3a2 protects AML cells from oxidative death and the synthetic lethality of ferroptosis inducers

Author

Harvard University - Department of Stem Cell and Regenerative Biology, Harvard University - Harvard Stem Cell Institute, Massachusetts General Hospital - Center for Regenerative Medicine, Yusuf, Rushdia Z., Saez, Borja, Sharda, Azeem, Van Gastel, Nick, Yu, Vionnie W.C., Baryawno, Ninib, Scadden, Elizabeth W., Acharya, Sanket, Chattophadhyay, Shrikanta, Huang, Cherrie, Viswanathan, Vasanthi, S'aulis, Dana, Cobert, Julien, Sykes, David B., Keibler, Mark A., Das, Sudeshna, Hutchinson, John N., Churchill, Michael, Mukherjee, Siddhartha, Lee, Dongjun, Mercier, Francois, Doench, John, Bullinger, Lars, Logan, David J., Schreiber, Stuart, Stephanopoulos, Gregory, Rizzo, William B., Scadden, David T., Harvard University - Department of Stem Cell and Regenerative Biology, Harvard University - Harvard Stem Cell Institute, Massachusetts General Hospital - Center for Regenerative Medicine, Yusuf, Rushdia Z., Saez, Borja, Sharda, Azeem, Van Gastel, Nick, Yu, Vionnie W.C., Baryawno, Ninib, Scadden, Elizabeth W., Acharya, Sanket, Chattophadhyay, Shrikanta, Huang, Cherrie, Viswanathan, Vasanthi, S'aulis, Dana, Cobert, Julien, Sykes, David B., Keibler, Mark A., Das, Sudeshna, Hutchinson, John N., Churchill, Michael, Mukherjee, Siddhartha, Lee, Dongjun, Mercier, Francois, Doench, John, Bullinger, Lars, Logan, David J., Schreiber, Stuart, Stephanopoulos, Gregory, Rizzo, William B., and Scadden, David T.

Abstract

Metabolic alterations in cancer represent convergent effects of oncogenic mutations. We hypothesized that a metabolism-restricted genetic screen, comparing normal primary mouse hematopoietic cells and their malignant counterparts in an ex vivo system mimicking the bone marrow microenvironment, would define distinctive vulnerabilities in acute myeloid leukemia (AML). Leukemic cells, but not their normal myeloid counterparts, depended on the aldehyde dehydrogenase 3a2 (Aldh3a2) enzyme that oxidizes long-chain aliphatic aldehydes to prevent cellular oxidative damage. Aldehydes are by-products of increased oxidative phosphorylation and nucleotide synthesis in cancer and are generated from lipid peroxides underlying the non-caspase-dependent form of cell death, ferroptosis. Leukemic cell dependence on Aldh3a2 was seen across multiple mouse and human myeloid leukemias. Aldh3a2 inhibition was synthetically lethal with glutathione peroxidase-4 (GPX4) inhibition; GPX4 inhibition is a known trigger of ferroptosis that by itself minimally affects AML cells. Inhibiting Aldh3a2 provides a therapeutic opportunity and a unique synthetic lethality to exploit the distinctive metabolic state of malignant cells.

Published
2020

4. FIAT represses ATF4-mediated transcription to regulate bone mass in transgenic mice

Author

Yu, Vionnie W.C., Ambartsoumian, Gourgen, Verlinden, Lieve, Moir, Janet M., Prud'homme, Josee, Gauthier, Claude, Roughley, Peter J., and St-Arnaud, Rene

Subjects
Genetic transcription -- Research, Genetically modified mice -- Research, Cytology -- Research, Bones -- Density, Bones -- Research, Bones -- Genetic aspects, Biological sciences
Abstract

We report the characterization of factor inhibiting activating transcription factor 4 (ATF4)--mediated transcription (FIAT), a leucine zipper nuclear protein. FIAT interacted with ATF4 to inhibit binding of ATF4 to DNA and block ATF4-mediated transcription of the osteocalcin gene in vitro. Transgenic mice overexpressing FIAT in osteoblasts also had reduced osteocalcin gene expression and decreased bone mineral density, bone volume, mineralized volume, trabecular thickness, trabecular number, and decreased rigidity of long bones. Mineral homeostasis, osteoclast number and activity, and osteoblast proliferation and apoptosis were unchanged in transgenics. Expression of osteoblastic differentiation markers was largely unaffected and type 1 collagen synthesis was unchanged. Mineral apposition rate was reduced in transgenic mice, suggesting that the lowered bone mass was due to a decline in osteoblast activity. This cell-autonomous decrease in osteoblast activity was confirmed by measuring reduced alkaline phosphatase activity and mineralization in primary osteoblast cultures. These results show that FIAT regulates bone mass accrual and establish FIAT as a novel transcriptional regulator of osteoblastic function.

Published
2005

6. Epigenetic Memory Underlies Cell-Autonomous Heterogeneous Behavior of Hematopoietic Stem Cells

Author

Yu, Vionnie W.C., primary, Yusuf, Rushdia Z., additional, Oki, Toshihiko, additional, Wu, Juwell, additional, Saez, Borja, additional, Wang, Xin, additional, Cook, Colleen, additional, Baryawno, Ninib, additional, Ziller, Michael J., additional, Lee, Eunjung, additional, Gu, Hongcang, additional, Meissner, Alexander, additional, Lin, Charles P., additional, Kharchenko, Peter V., additional, and Scadden, David T., additional

Published
2017
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8. Epigenetic Memory Underlies Cell-Autonomous Heterogeneous Behavior of Hematopoietic Stem Cells

Author

Yu, Vionnie W.C., primary, Yusuf, Rushdia Z., additional, Oki, Toshihiko, additional, Wu, Juwell, additional, Saez, Borja, additional, Wang, Xin, additional, Cook, Colleen, additional, Baryawno, Ninib, additional, Ziller, Michael J., additional, Lee, Eunjung, additional, Gu, Hongcang, additional, Meissner, Alexander, additional, Lin, Charles P., additional, Kharchenko, Peter V., additional, and Scadden, David T., additional

Published
2016
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9. Aldehyde dehydrogenase 3a2 protects AML cells from oxidative death and the synthetic lethality of ferroptosis inducers

Author

Yusuf, Rushdia Zareen, Saez, Borja, Sharda, Azeem, van Gastel, Nick, Yu, Vionnie W.C., Baryawno, Ninib, Scadden, Elizabeth W., Acharya, Sanket, Chattophadhyay, Shrikanta, Huang, Cherrie, Viswanathan, Vasanthi, S'aulis, Dana, Cobert, Julien, Sykes, David B., Keibler, Mark A., Das, Sudeshna, Hutchinson, John N., Churchill, Michael, Mukherjee, Siddhartha, Lee, Dongjun, Mercier, Francois, Doench, John, Bullinger, Lars, Logan, David J., Schreiber, Stuart, Stephanopoulos, Gregory, Rizzo, William B., and Scadden, David T.

Abstract

Metabolic alterations in cancer represent convergent effects of oncogenic mutations. We hypothesized that a metabolism-restricted genetic screen, comparing normal primary mouse hematopoietic cells and their malignant counterparts in an ex vivo system mimicking the bone marrow microenvironment, would define distinctive vulnerabilities in acute myeloid leukemia (AML). Leukemic cells, but not their normal myeloid counterparts, depended on the aldehyde dehydrogenase 3a2 (Aldh3a2) enzyme that oxidizes long-chain aliphatic aldehydes to prevent cellular oxidative damage. Aldehydes are by-products of increased oxidative phosphorylation and nucleotide synthesis in cancer and are generated from lipid peroxides underlying the non–caspase-dependent form of cell death, ferroptosis. Leukemic cell dependence on Aldh3a2was seen across multiple mouse and human myeloid leukemias. Aldh3a2 inhibition was synthetically lethal with glutathione peroxidase-4 (GPX4) inhibition; GPX4 inhibition is a known trigger of ferroptosis that by itself minimally affects AML cells. Inhibiting Aldh3a2 provides a therapeutic opportunity and a unique synthetic lethality to exploit the distinctive metabolic state of malignant cells.

Published
2020
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10. Cell-State-Specific Metabolic Dependency in Hematopoiesis and Leukemogenesis

Author

Massachusetts Institute of Technology. Department of Biology, Koch Institute for Integrative Cancer Research at MIT, Israelsen, William James, Vander Heiden, Matthew G., Wang, Ying-Hua, Lee, Dongjun, Yu, Vionnie W.C., Jeanson, Nathaniel T., Clish, Clary B., Cantley, Lewis C., Scadden, David T., Massachusetts Institute of Technology. Department of Biology, Koch Institute for Integrative Cancer Research at MIT, Israelsen, William James, Vander Heiden, Matthew G., Wang, Ying-Hua, Lee, Dongjun, Yu, Vionnie W.C., Jeanson, Nathaniel T., Clish, Clary B., Cantley, Lewis C., and Scadden, David T.

Abstract

The balance between oxidative and non-oxidative glucose metabolism is essential for a number of pathophysiological processes. By deleting enzymes that affect aerobic glycolysis with different potencies, we examine how modulating glucose metabolism specifically affects hematopoietic and leukemic cell populations. We find that deficiency in the M2 pyruvate kinase isoform (PKM2) reduces levels of metabolic intermediates important for biosynthesis and impairs progenitor function without perturbing hematopoietic stem cells (HSC), whereas lactate dehydrogenase-A (LDHA) deletion significantly inhibits the function of both HSC and progenitors during hematopoiesis. In contrast, leukemia initiation by transforming alleles putatively affecting either HSC or progenitors is inhibited in the absence of either PKM2 or LDHA, indicating that the cell state-specific responses to metabolic manipulation in hematopoiesis do not apply to the setting of leukemia. This finding suggests that fine-tuning the level of glycolysis may be therapeutically explored for treating leukemia while preserving HSC function., National Institutes of Health (U.S.) (Grants P30CA147882 and R01CA168653), Smith Family Foundation, Burroughs Wellcome Fund, Virginia and D.K. Ludwig Fund for Cancer Research, Damon Runyon Cancer Research Foundation

Published
2016

13. CRISPR/Cas9 Gene-Edited Hematopoietic Stem Cell Therapy for Sickle Cell Disease

Author

Yu, Vionnie W.C., Liu, Yi, Curran, Matthew, Zhang, Pu, Snead, Jennifer, Schmedt, Christian, Yang, Yi, Lin, Victor Guosheng, Tschantz, William R, Quinn, Lisa, Russ, Carsten, Clarkson, Scott, Janiak, Amy, Stewart, Morag, Mulumba, Yanick, Lescarbeau, Reynald, Murray, Brad, Seitzer, Jessica, Strapps, Walter, Huang, Hon-Ren, Sloan, Kevin, Mickanin, Craig S, Klickstein, Lloyd, and Stevenson, Susan

Published
2017
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16. Specific bone cells produce DLL4 to generate thymus-seeding progenitors from bone marrow

Author

Yu, Vionnie W.C., primary, Saez, Borja, additional, Cook, Colleen, additional, Lotinun, Sutada, additional, Pardo-Saganta, Ana, additional, Wang, Ying-Hua, additional, Lymperi, Stefania, additional, Ferraro, Francesca, additional, Raaijmakers, Marc H.G.P., additional, Wu, Joy Y., additional, Zhou, Lan, additional, Rajagopal, Jayaraj, additional, Kronenberg, Henry M., additional, Baron, Roland, additional, and Scadden, David T., additional

Published
2015
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17. Loss of Notch Receptor-Ligand Engagement Leads to Increased Hematopoietic Stem and Progenitor Cell Egress and Mobilization

Author

Zhou, Lan, primary, Wang, Weihuan, additional, Zimmerman, Grant, additional, Myers, Jay, additional, Huang, Yuanshuai, additional, Yu, Vionnie W.C., additional, Huang, Dan, additional, Yu, Shuiliang, additional, Wang, Yiwei, additional, Huang, Xiaoran, additional, Shim, Jeongsup, additional, Yan, Minhong, additional, Lowe, John, additional, Xin, Wei, additional, Stanley, Pamela, additional, Scadden, David T., additional, Huang, Alex Y, additional, and Siebel, Christian W., additional

Published
2014
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18. Sex steroid blockade enhances thymopoiesis by modulating Notch signaling

Author

Velardi, Enrico, primary, Tsai, Jennifer J., additional, Holland, Amanda M., additional, Wertheimer, Tobias, additional, Yu, Vionnie W.C., additional, Zakrzewski, Johannes L., additional, Tuckett, Andrea Z., additional, Singer, Natalie V., additional, West, Mallory L., additional, Smith, Odette M., additional, Young, Lauren F., additional, Kreines, Fabiana M., additional, Levy, Emily R., additional, Boyd, Richard L., additional, Scadden, David T., additional, Dudakov, Jarrod A., additional, and van den Brink, Marcel R.M., additional

Published
2014
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22. Aldehyde Dehydrogenase 3a2 (Aldh3a2) Represents a Distinct Metabolic Vulnerability in MLL-AF9 AML Leukemia Initiating Cells

Author

Yusuf, Rushdia Z., primary, Acharya, Sanket S., additional, Yu, Vionnie W.C., additional, Saez, Borja, additional, Cobert, Julien M, additional, Doench, John, additional, Bullinger, Lars, additional, S'aulis, Dana, additional, Lee, Dongjun, additional, Palchaudhuri, Rahul, additional, Uzosike, Akachimere C., additional, Duvet, Mildred, additional, Logan, David J., additional, Das, Sudeshna, additional, Cook, Colleen M, additional, Churchill, Michael, additional, Scadden, Elizabeth, additional, Warraich, Gohar, additional, Liu, Hao, additional, Chattopadhyay, Shrikanta, additional, Brown, Adam, additional, Sykes, Stephen M., additional, Sykes, David B., additional, Mercier, Francois, additional, Carpenter, Anne E., additional, Armstrong, Scott A., additional, Vander Heiden, Matthew, additional, Ebert, Benjamin L., additional, Kung, Andrew L., additional, Rizzo, William B., additional, Mukherjee, Siddhartha, additional, and Scadden, David T., additional

Published
2012
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23. Hematopoietic Stem/Progenitor Cell Retention in the Bone Marrow Depends On Tissue Specific Heparan Sulfate Proteoglycans

Author

Saez, Borja, primary, Ferraro, Francesca, additional, Yusuf, Rushdia Z., additional, Cook, Colleen M, additional, Sykes, Stephen M., additional, Pardo, Ana, additional, Yu, Vionnie W.C., additional, Lotinun, Sutada, additional, Palchaudhuri, Rahul, additional, Lee, Dongjun, additional, Lymperi, Stefania, additional, Day, Robyn, additional, Vasic, Radovan, additional, Acharya, Sanket S., additional, Baron, Roland, additional, Wagers, Amy J., additional, and Scadden, David T., additional

Published
2012
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