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...
Saved in:
Main Author: | |
---|---|
Format: | Book Chapter |
Published: |
Firenze University Press
2017
|
Online Access: | Get Fullteks DOAB: description of the publication |
Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
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 |
---|---|
Physical Description: | 1 electronic resource (80 p.) |
ISBN: | 978-88-6453-565-4 9788864535654 |
Access: | Open Access |