Study of intracellular signaling pathways in Chronic Myeloproliferative Neoplasms
A gain-of-function mutation in Janus kinase 2 (JAK2V617F) is at the basis of the majority of chronic myeloproliferative neoplasms (MPN). Enhanced activation of other downstream pathways including the PI3K/mTOR pathway has been documented as well. In this study we evaluated the effects of JAK1/2 inhi...
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Format: | Book Chapter |
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Firenze University Press
2017
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Online Access: | Get Fullteks DOAB: description of the publication |
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LEADER | 01647naaaa2200205uu 4500 | ||
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001 | doab_20_500_12854_60210 | ||
005 | 20210212 | ||
020 | |a 978-88-6453-565-4 | ||
020 | |a 9788864535654 | ||
024 | 7 | |a 10.36253/978-88-6453-565-4 |c doi | |
042 | |a dc | ||
100 | 1 | |a Serena Martinelli |4 auth | |
245 | 1 | 0 | |a Study of intracellular signaling pathways in Chronic Myeloproliferative Neoplasms |
260 | |b Firenze University Press |c 2017 | ||
300 | |a 1 electronic resource (80 p.) | ||
506 | 0 | |a Open Access |2 star |f Unrestricted online access | |
520 | |a A gain-of-function mutation in Janus kinase 2 (JAK2V617F) is at the basis of the majority of chronic myeloproliferative neoplasms (MPN). Enhanced activation of other downstream pathways including the PI3K/mTOR pathway has been documented as well. In this study we evaluated the effects of JAK1/2 inhibitors, alone and in combination with mTOR, with a dual mTOR/PI3K inhibitor and with a pan PI3K inhibitor in in-vitro and in-vivo MPN models. Our findings of strong synergy between the JAK2 inhibitors and mTOR/PI3K inhibitor suggested that we might be able to administer these drugs at lower concentrations than when the drugs are used individually. This provides a framework for combination trials using compounds in patients with myeloproliferative neoplasms | ||
540 | |a Creative Commons |f https://creativecommons.org/licenses/by/4.0/ |2 cc |4 https://creativecommons.org/licenses/by/4.0/ | ||
856 | 4 | 0 | |a www.oapen.org |u https://www.fupress.com/redir.ashx?RetUrl=3501_14477.pdf |7 0 |z Get Fullteks |
856 | 4 | 0 | |a www.oapen.org |u https://directory.doabooks.org/handle/20.500.12854/60210 |7 0 |z DOAB: description of the publication |