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Absence of mutations in the granulocyte colony‐stimulating factor (G‐CSF) receptor gene in patients with myelodysplastic syndrome/acute myeloblastic leukaemia occurring after treatment of aplastic anaemia with G‐CSF
Author(s) -
Kudo Kazuko,
Nagai Hirokazu,
Numata Shinichiro,
Ichihara Masatoshi,
Kinoshita Tomohiro,
Horibe Keizo,
Kato Koji,
Matsuyama Takaharu,
Kodera Yoshihisa,
Kojima Seiji
Publication year - 2000
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1111/j.1365-2141.2000.02370.x
Subject(s) - congenital neutropenia , granulocyte colony stimulating factor , acute myeloblastic leukemia , aplastic anemia , medicine , granulocyte colony stimulating factor receptor , neutropenia , myelodysplastic syndromes , granulocyte , immunology , filgrastim , leukemia , chemotherapy , bone marrow
The development of myelodysplastic syndrome/acute myeloblastic leukaemia (MDS/AML) has been reported in patients with aplastic anaemia (AA) after administration of recombinant human granulocyte colony‐stimulating factor (rhG‐CSF). Similarly, patients with severe congenital neutropenia (SCN) have an increased risk of developing MDS/AML after treatment with rhG‐CSF. Point mutations in the G‐CSF receptor gene are found in about 20% of SCN patients who are predisposed to MDS/AML. We investigated the occurrence of mutations in the G‐CSF receptor in eight patients with AA who developed MDS/AML. No mutations were detected around the cytoplasmic domain of the gene in our patients, indicating that the mechanisms of clonal evolution to MDS/AML in patients with AA might be different from those with SCN.