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 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
- DOI: 10.36253/978-88-6453-565-4
- Series: Premio Tesi di Dottorato
- Scientific Board
- Language: English
- Subjects: Biology
University of Florence, Italy
- Publication Year: 2017
- Pages: 80
- eISBN: 978-88-6453-565-4
- Content License: CC BY 4.0
- © 2017 Author(s)
- Publication Year: 2017
- Pages: 80
- ISBN: 978-88-6453-564-7
- Content License: CC BY 4.0
- © 2017 Author(s)
Bibliographic Information
Book Title
Study of intracellular signaling pathways in Chronic Myeloproliferative Neoplasms
Authors
Serena Martinelli
Peer Reviewed
Number of Pages
80
Publication Year
2017
Copyright Information
© 2017 Author(s)
Content License
Metadata License
Publisher Name
Firenze University Press
DOI
10.36253/978-88-6453-565-4
ISBN Print
978-88-6453-564-7
eISBN (pdf)
978-88-6453-565-4
eISBN (xml)
978-88-9273-168-4
Series Title
Premio Tesi di Dottorato
Series ISSN
2612-8039
Series E-ISSN
2612-8020
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