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Lipocalin‐2 is associated with modulation of disease phenotype in a patient with concurrent JAK2 ‐V617F and BCR‐ABL mutation
Author(s) -
Nadarajan Veera S.,
Ang ChowHiang,
Bee PingChong
Publication year - 2012
Publication title -
european journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.904
H-Index - 84
eISSN - 1600-0609
pISSN - 0902-4441
DOI - 10.1111/j.1600-0609.2011.01712.x
Subject(s) - polycythaemia , phenotype , abl , biology , cancer research , imatinib , imatinib mesylate , jak2 v617f , dominance (genetics) , myeloid leukemia , breakpoint cluster region , philadelphia chromosome , mutation , receptor , medicine , genetics , chromosomal translocation , gene , tyrosine kinase
We investigated the role of lipocalin‐2 (LCN‐2) and its receptor (SLC22A17) in mediating clonal dominance in a patient with both BCR‐ABL and JAK2 ‐V617F mutations. LCN‐2 mRNA showed a near 50‐fold increase in expression, accompanied by down‐regulation of SLC22A17, coinciding with increase in BCR‐ABL transcripts, loss of JAK2 ‐V617F and change of clinical phenotype from polycythaemia vera to chronic myeloid leukaemia. These changes were reversed after commencing imatinib mesylate. Consistent with experimental studies, BCR‐ABL+ cells express LCN‐2 leading to suppression of BCR‐ABL‐ cells and explain their eventual dominance when occurring together with JAK2 ‐V617F.