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Giovanni Barosi

Researcher at University of Pavia

Publications -  352
Citations -  21433

Giovanni Barosi is an academic researcher from University of Pavia. The author has contributed to research in topics: Myelofibrosis & Essential thrombocythemia. The author has an hindex of 69, co-authored 334 publications receiving 19225 citations.

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Identification of patients with poorer survival in primary myelofibrosis based on the burden of JAK2V617F mutated allele.

TL;DR: It is concluded that a low JAK2V617F allele burden at diagnosis is preferentially associated with a myelodepletive rather than myeloproliferative phenotype and represents an independent factor associated with shortened survival in patients with PMF.
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Italian Society of Hematology practice guidelines for the management of iron overload in thalassemia major and related disorders

TL;DR: The Italian Society of Hematology appointed a panel of experts to produce clinical practice-guidelines for the management of iron overload in thalassemia major and related disorders, and the resulting recommendations advise about which examination to carry out in order to planIron chelation therapy, when to start iron chelation, which iron chelator to choose in regularly transfused patients, how to monitor iron chelated therapy, and when and how to switch standard therapy.
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Pivotal contributions of megakaryocytes to the biology of idiopathic myelofibrosis

TL;DR: MK hyperplasia in IMF is likely a consequence of both the increased ability of IMF progenitor cells to generate MKs and a decreased rate of MK apoptosis, which contribute to the development of many pathological epiphenomena associated with IMF.
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Life expectancy and prognostic factors in the classic BCR/ABL-negative myeloproliferative disorders

TL;DR: Among the ‘classic’ BCR/ABL-negative chronic myeloproliferative disorders, primary myelofibrosis (PMF) is associated with a substantial life-expectancy reduction and the importance of higher leukocyte counts in thrombosis development has been recently pointed out in ET and PV, where a role for mutated JAK2 allele burden has been noted.