Hydroxyurea (HU) is effective in reducing JAK2V617F mutated clone size in the peripheral blood of essential thrombocythemia (ET) and polycythemia vera (PV) patients.
Ph-negative chronic myeloproliferative disorders (Ph(neg)cMPD) are treated according to the estimated vascular risk. The recent discovery of V617F point mutation of the JAK2 kinase, which frequently occurs in these diseases, has not changed their management so far. However, emerging data tend to support a prothrombotic role for the mutation, along with a better response of JAK2V617F mutated patients to hydroxyurea treatment. Our data further support this notion.
Spanoudakis
Emmanouil
E
Department of Haematology, Democritus University of Thrace, Medical School, Area of Dragana, Alexandroupolis, Greece.
Bazdiara
Ioanna
I
Kotsianidis
Ioannis
I
Margaritis
Dimitrios
D
Goutzouvelidis
Aggelos
A
Christoforidou
Anna
A
Tsatalas
Costas
C
Bourikas
George
G
D001853:Bone Marrow; D002999:Clone Cells / Q000187:drug effects / Q000473:pathology; D006412:Hematopoietic Stem Cells; D006801:Humans; D006918:Hydroxyurea / Q000008:administration & dosage / Q000494:pharmacology*; D053614:Janus Kinase 2 / Q000235:genetics*; D020125:Mutation, Missense; D011087:Polycythemia Vera / Q000097:blood / Q000188:drug therapy* / Q000473:pathology; D013920:Thrombocythemia, Essential / Q000097:blood / Q000188:drug therapy* / Q000473:pathology; D019851:Thrombophilia / Q000235:genetics; D016896:Treatment Outcome
D053614:Janus Kinase 2; D006918:Hydroxyurea