In:
Oncology Research and Treatment, S. Karger AG, Vol. 39, No. 6 ( 2016), p. 384-387
Abstract:
〈 b 〉 〈 i 〉 Background: 〈 /i 〉 〈 /b 〉 Iron overload is a common problem in patients with primary myelofibrosis and anemia due to transfusion dependency. This results in organ damage and toxic effects on hematopoietic cells in the bone marrow. At present, iron chelation therapy is not recommended in patients with myeloproliferative syndromes. 〈 b 〉 〈 i 〉 Case Report: 〈 /i 〉 〈 /b 〉 We describe a very interesting development in a patient with primary myelofibrosis receiving iron chelation. Transfusion independency and a nearly complete histological remission of the underlying disease occurred within a few weeks of therapy. In addition, a change in molecular genetic findings was observed. Initially a 〈 i 〉 JAK2 〈 /i 〉 and a 〈 i 〉 U2AF1 〈 /i 〉 mutation were detected in the core biopsy. During and after therapy the 〈 i 〉 U2AF1 〈 /i 〉 mutation progressed, whereas the 〈 i 〉 JAK2 〈 /i 〉 mutation could no longer be verified. 〈 b 〉 〈 i 〉 Conclusion: 〈 /i 〉 〈 /b 〉 The improvement in hematopoiesis might results from reduction of oxidative stress on hematopoietic progenitor cells or other unclear deferasirox-mediated effects, whereas the reason for the change in molecular genetic findings is unclear. It appears that deferasirox might have a modulating effect on JAK2-kinase mutations. However, further investigation of selective molecular suppression properties of deferasirox are warranted.
Type of Medium:
Online Resource
ISSN:
2296-5270
,
2296-5262
Language:
English
Publisher:
S. Karger AG
Publication Date:
2016
detail.hit.zdb_id:
2749752-5
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