Study of intracellular signaling pathways in Chronic Myeloproliferative Neoplasms / / Serena Martinelli.
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:
| Superior document: | Premio Tesi di Dottorato |
|---|---|
| VerfasserIn: | |
| Place / Publishing House: | Florence : : Firenze University Press,, 2017. |
| Year of Publication: | 2017 |
| Language: | English |
| Series: | Premio tesi di dottorato.
|
| Physical Description: | 1 online resource (80 pages). |
| 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. |
|---|---|
| Hierarchical level: | Monograph |
| Statement of Responsibility: | Serena Martinelli. |