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...
| Main Author: | |
|---|---|
| Format: | eBook |
| Language: | English |
| Published: |
Florence
Firenze University Press
2017
|
| Series: | Premio Tesi di Dottorato
|
| Subjects: | |
| Online Access: | |
| Collection: | OAPEN - Collection details see MPG.ReNa |
| Summary: | 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 |
|---|---|
| Item Description: | Creative Commons (cc), https://creativecommons.org/licenses/by/4.0/ |
| Physical Description: | 80 p. |
| ISBN: | 9788892731684 9788864535654 9788864535647 978-88-6453-565-4 |