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4 results on '"Ito, Moriko"'

1. A conditional inducible JAK2V617F transgenic mouse model reveals myeloproliferative disease that is reversible upon switching off transgene expression

Author

Chapeau, Emilie A., primary, Mandon, Emeline, additional, Gill, Jason, additional, Romanet, Vincent, additional, Ebel, Nicolas, additional, Powajbo, Violetta, additional, Andraos-Rey, Rita, additional, Qian, Zhiyan, additional, Kininis, Miltos, additional, Zumstein-Mecker, Sabine, additional, Ito, Moriko, additional, Hynes, Nancy E., additional, Tiedt, Ralph, additional, Hofmann, Francesco, additional, Eshkind, Leonid, additional, Bockamp, Ernesto, additional, Kinzel, Bernd, additional, Mueller, Matthias, additional, Murakami, Masato, additional, Baffert, Fabienne, additional, and Radimerski, Thomas, additional

Published
2019
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2. A conditional inducible JAK2V617F transgenic mouse model reveals myeloproliferative disease that is reversible upon switching off transgene expression.

Author

Chapeau, Emilie A., Mandon, Emeline, Gill, Jason, Romanet, Vincent, Ebel, Nicolas, Powajbo, Violetta, Andraos-Rey, Rita, Qian, Zhiyan, Kininis, Miltos, Zumstein-Mecker, Sabine, Ito, Moriko, Hynes, Nancy E., Tiedt, Ralph, Hofmann, Francesco, Eshkind, Leonid, Bockamp, Ernesto, Kinzel, Bernd, Mueller, Matthias, Murakami, Masato, and Baffert, Fabienne

Subjects
TRANSGENIC mice, HEMATOPOIETIC stem cells, POLYCYTHEMIA vera, BONE marrow cells, TRANSGENE expression, DISEASES
Abstract

Aberrant activation of the JAK/STAT pathway is thought to be the critical event in the pathogenesis of the chronic myeloproliferative neoplasms, polycythemia vera, essential thrombocythemia and primary myelofibrosis. The most frequent genetic alteration in these pathologies is the activating JAK2V617F mutation, and expression of the mutant gene in mouse models was shown to cause a phenotype resembling the human diseases. Given the body of genetic evidence, it has come as a sobering finding that JAK inhibitor therapy only modestly suppresses the JAK2V617F allele burden, despite showing clear benefits in terms of reducing splenomegaly and constitutional symptoms in patients. To gain a better understanding if JAK2V617F is required for maintenance of myeloproliferative disease once it has evolved, we generated a conditional inducible transgenic JAK2V617F mouse model using the SCL-tTA-2S tet-off system. Our model corroborates that expression of JAK2V617F in hematopoietic stem and progenitor cells recapitulates key hallmarks of human myeloproliferative neoplasms, and exhibits gender differences in disease manifestation. The disease was found to be transplantable, and importantly, reversible when transgenic JAK2V617F expression was switched off. Our results indicate that mutant JAK2V617F-specific inhibitors should result in profound disease modification by disabling the myeloproliferative clone bearing mutant JAK2. [ABSTRACT FROM AUTHOR]

Published
2019
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3. Fibroblast Growth Factor Receptors as Novel Therapeutic Targets in SNF5-Deleted Malignant Rhabdoid Tumors

Author

Wöhrle, Simon, primary, Weiss, Andreas, additional, Ito, Moriko, additional, Kauffmann, Audrey, additional, Murakami, Masato, additional, Jagani, Zainab, additional, Thuery, Anne, additional, Bauer-Probst, Beatrice, additional, Reimann, Flavia, additional, Stamm, Christelle, additional, Pornon, Astrid, additional, Romanet, Vincent, additional, Guagnano, Vito, additional, Brümmendorf, Thomas, additional, Sellers, William R., additional, Hofmann, Francesco, additional, Roberts, Charles W. M., additional, and Graus Porta, Diana, additional

Published
2013
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4. The Tyrosine Phosphatase PTPN14 Is a Negative Regulator of YAP Activity

Author

Michaloglou, Chrysiis, primary, Lehmann, Waltraut, additional, Martin, Typhaine, additional, Delaunay, Clara, additional, Hueber, Andreas, additional, Barys, Louise, additional, Niu, Honglin, additional, Billy, Eric, additional, Wartmann, Markus, additional, Ito, Moriko, additional, Wilson, Christopher J., additional, Digan, Mary Ellen, additional, Bauer, Andreas, additional, Voshol, Hans, additional, Christofori, Gerhard, additional, Sellers, William R., additional, Hofmann, Francesco, additional, and Schmelzle, Tobias, additional

Published
2013
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