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Study of intracellular signaling pathways in Chronic Myeloproliferative Neoplasms
Serena Martinelli
2017
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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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Keywords
- Biochemistry
- Biology, Life Sciences
- Mathematics & science
- medicine
- Molecular biology
- Nursing & ancillary services
- Pharmacy / dispensing
- Pre-clinical medicine: basic sciences
- thema EDItEUR::M Medicine and Nursing::MF Pre-clinical medicine: basic sciences
- thema EDItEUR::M Medicine and Nursing::MQ Nursing and ancillary services::MQP Pharmacy / dispensing
- thema EDItEUR::P Mathematics and Science::PS Biology, life sciences
- thema EDItEUR::P Mathematics and Science::PS Biology, life sciences::PSB Biochemistry
- thema EDItEUR::P Mathematics and Science::PS Biology, life sciences::PSD Molecular biology
Links
DOI: 10.36253/978-88-6453-565-4Editions