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18 results on '"Staser, Karl W."'

5. Imatinib mesylate for plexiform neurofibromas in patients with neurofibromatosis type 1: a phase 2 trial

Author

Robertson, Kent A, Nalepa, Grzegorz, Yang, Feng-Chun, Bowers, Daniel C, Ho, Chang Y, Hutchins, Gary D, Croop, James M, Vik, Terry A, Denne, Scott C, Parada, Luis F, Hingtgen, Cynthia M, Walsh, Laurence E, Yu, Menggang, Pradhan, Kamnesh R, Edwards-Brown, Mary K, Cohen, Mervyn D, Fletcher, James W, Travers, Jeffrey B, Staser, Karl W, Lee, Melissa W, Sherman, Marcie R, Davis, Cynthia J, Miller, Lucy C, Ingram, David A, and Clapp, D Wade

Published
2012
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8. Modeling Sézary Syndrome for Immunophenotyping and Anti-Tumor Effect of Ucart and Long-Acting Interleukin-7 Combination Therapy

Author

Staser, Karl W., primary, Cooper, Matthew L., additional, Choi, Jaebok, additional, Chukka, Anand, additional, Ashami, Kidist, additional, Niswonger, Jessica, additional, Park, Jaehan, additional, Lee, Byung Ha, additional, Li, Shunqiang, additional, Cashen, Amanda F, additional, Musiek, Amy, additional, and DiPersio, John F., additional

Published
2018
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12. An Off-the-Shelf™ Fratricide-Resistant CAR-T for the Treatment of T Cell Hematologic Malignancies

Author

Cooper, Matt L, primary, Choi, Jaebok, additional, Staser, Karl W., additional, Ritchey, Julie, additional, Niswonger, Jessica, additional, Eckardt, Kayla, additional, Rettig, Michael P, additional, Bing, Wang, additional, Eissenberg, Linda G, additional, Ghobadi, Armin, additional, Gehrs, Leah, additional, Prior, Julie, additional, Achilefu, Samuel, additional, Miller, Christopher A, additional, Fronick, Catrina, additional, O'Neal, Julie, additional, Gao, Feng, additional, Weinstock, David M., additional, Gutierrez, Alejandro, additional, Fulton, Robert S, additional, and DiPersio, John F, additional

Published
2017
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13. Nf1 haploinsufficiency alters myeloid lineage commitment and function, leading to deranged skeletal homeostasis

Author

Rhodes, Steven D., Yang, Hao, Dong, Ruizhi, Menon, Keshav, He, Yongzheng, Li, Zhaomin, Chen, Shi, Staser, Karl W., Jiang, Li, Wu, Xiaohua, Yang, Xianlin, Peng, Xianghong, Mohammad, Khalid S., Guise, Theresa A., Xu, Mingjiang, and Yang, Feng-Chun

Subjects
congenital, hereditary, and neonatal diseases and abnormalities, Neurofibromin 1, Osteoclasts, Mice, Transgenic, Haploinsufficiency, Osteolysis, eye diseases, Article, nervous system diseases, Proto-Oncogene Proteins p21(ras), Mice, Proto-Oncogene Proteins, Trans-Activators, Animals, Humans, Osteoporosis, neoplasms, Myeloid Progenitor Cells
Abstract

While nullizygous loss of NF1 leads to myeloid malignancies, haploinsufficient loss of NF1 (Nf1) has been shown to contribute to osteopenia and osteoporosis which occurs in approximately 50 percent of neurofibromatosis type 1 (NF1) patients. Bone marrow mononuclear cells of haploinsufficient NF1 patients and Nf1+/- mice exhibit increased osteoclastogenesis and accelerated bone turnover, however the culprit hematopoietic lineages responsible for perpetuating these osteolytic manifestations have yet to be elucidated. Here we demonstrate that conditional inactivation of a single Nf1 allele within the myeloid progenitor cell population (Nf1-LysM) is necessary and sufficient to promote multiple osteoclast gain-in-functions, resulting in enhanced osteoclastogenesis and accelerated osteoclast bone lytic activity in response to pro-resorptive challenge in vivo. Surprisingly, mice conditionally Nf1 heterozygous in mature, terminally differentiated osteoclasts (Nf1-Ctsk) do not exhibit any of these skeletal phenotypes, indicating a critical requirement for Nf1 haploinsufficiency at a more primitive/progenitor stage of myeloid development in perpetuating osteolytic activity. We further identified p21Ras dependent hyper-phosphorylation of Pu.1 within the nucleus of Nf1 haploinsufficent myelomoncytic osteoclast precursors, providing a novel therapeutic target for the potential treatment of NF1 associated osteolytic manifestations.

Published
2015

15. Nf1Haploinsufficiency Alters Myeloid Lineage Commitment and Function, Leading to Deranged Skeletal Homeostasis

Author

Rhodes, Steven D, primary, Yang, Hao, additional, Dong, Ruizhi, additional, Menon, Keshav, additional, He, Yongzheng, additional, Li, Zhaomin, additional, Chen, Shi, additional, Staser, Karl W, additional, Jiang, Li, additional, Wu, Xiaohua, additional, Yang, Xianlin, additional, Peng, Xianghong, additional, Mohammad, Khalid S, additional, Guise, Theresa A, additional, Xu, Mingjiang, additional, and Yang, Feng-Chun, additional

Published
2015
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16. Hyperactive Transforming Growth Factor-β1 Signaling Potentiates Skeletal Defects in a Neurofibromatosis Type 1 Mouse Model

Author

Rhodes, Steven D, primary, Wu, Xiaohua, additional, He, Yongzheng, additional, Chen, Shi, additional, Yang, Hao, additional, Staser, Karl W, additional, Wang, Jiapeng, additional, Zhang, Ping, additional, Jiang, Chang, additional, Yokota, Hiroki, additional, Dong, Ruizhi, additional, Peng, Xianghong, additional, Yang, Xianlin, additional, Murthy, Sreemala, additional, Azhar, Mohamad, additional, Mohammad, Khalid S, additional, Xu, Mingjiang, additional, Guise, Theresa A, additional, and Yang, Feng-Chun, additional

Published
2013
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17. Nf1 Haploinsufficiency Alters Myeloid Lineage Commitment and Function, Leading to Deranged Skeletal Homeostasis.

Author

Rhodes, Steven D, Yang, Hao, Dong, Ruizhi, Menon, Keshav, He, Yongzheng, Li, Zhaomin, Chen, Shi, Staser, Karl W, Jiang, Li, Wu, Xiaohua, Yang, Xianlin, Peng, Xianghong, Mohammad, Khalid S, Guise, Theresa A, Xu, Mingjiang, and Yang, Feng-Chun

Abstract

ABSTRACT Although nullizygous loss of NF1 leads to myeloid malignancies, haploinsufficient loss of NF1 ( Nf1) has been shown to contribute to osteopenia and osteoporosis which occurs in approximately 50% of neurofibromatosis type 1 (NF1) patients. Bone marrow mononuclear cells of haploinsufficient NF1 patients and Nf1+/- mice exhibit increased osteoclastogenesis and accelerated bone turnover; however, the culprit hematopoietic lineages responsible for perpetuating these osteolytic manifestations have yet to be elucidated. Here we demonstrate that conditional inactivation of a single Nf1 allele within the myeloid progenitor cell population ( Nf1-LysM) is necessary and sufficient to promote multiple osteoclast gains-in-function, resulting in enhanced osteoclastogenesis and accelerated osteoclast bone lytic activity in response to proresorptive challenge in vivo. Surprisingly, mice conditionally Nf1 heterozygous in mature, terminally differentiated osteoclasts ( Nf1-Ctsk) do not exhibit any of these skeletal phenotypes, indicating a critical requirement for Nf1 haploinsufficiency at a more primitive/progenitor stage of myeloid development in perpetuating osteolytic activity. We further identified p21Ras-dependent hyperphosphorylation of Pu.1 within the nucleus of Nf1 haploinsufficient myelomonocytic osteoclast precursors, providing a novel therapeutic target for the potential treatment of NF1 associated osteolytic manifestations. © 2015 American Society for Bone and Mineral Research [ABSTRACT FROM AUTHOR]

Published
2015
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