Study of intracellular signaling pathways in Chronic Myeloproliferative Neoplasms

Bibliographic Details
Title: Study of intracellular signaling pathways in Chronic Myeloproliferative Neoplasms
Authors: Martinelli, Serena
Publisher Information: Florence: Firenze University Press, 2017.
Publication Year: 2017
More Details: 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
Document Type: eBook
File Description: image/jpeg
Language: English
ISBN: 978-88-6453-565-4
978-88-6453-564-7
978-88-927-3168-4
ISSN: 2612-8020
Relation: Premio Tesi di Dottorato
DOI: 10.36253/978-88-6453-565-4
Access URL: https://directory.doabooks.org/handle/20.500.12854/83462
https://library.oapen.org/handle/20.500.12657/55390
https://library.oapen.org/bitstream/20.500.12657/55390/1/9788864535654.pdf
Rights: open access
Attribution 4.0 International
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URL: https://creativecommons.org/licenses/by/4.0/
Notes: ONIX_20220531_9788864535654_674

OCN: 1229607373
Accession Number: edsdob.20.500.12854.83462
Database: Directory of Open Access Books
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  Data: 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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