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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| 第一著者: | |
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| フォーマット: | 電子媒体 図書の章 |
| 言語: | 英語 |
| 出版事項: |
Florence
Firenze University Press
2017
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| シリーズ: | Premio Tesi di Dottorato
60 |
| 主題: | |
| オンライン･アクセス: | OAPEN Library: download the publication OAPEN Library: description of the publication |
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| 要約: | 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 |
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| 物理的記述: | 1 electronic resource (80 p.) |
| ISBN: | 978-88-6453-565-4 9788864535654 9788864535647 9788892731684 |
| アクセス: | Open Access |