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Study of intracellular signaling pathways in chronic myeloproliferative neoplasms

2017 - Firenze University Press

75 p. : ill.

  • 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.
  • Serena Martinelliobtained the PhD title in Biomedical Science at Florence University in 2016. She is co-author in several articles and she is listed as the leading author in one of them. Her technical skills and competences are cellular biology, molecular biology and mouse models. [Publisher's text].
  • Includes bibliographical references.