期刊
INTERNATIONAL JOURNAL OF HEMATOLOGY
卷 89, 期 4, 页码 422-430出版社
SPRINGER JAPAN KK
DOI: 10.1007/s12185-009-0286-5
关键词
Gfi1b; Gfi1; Imatinib; BCR-ABL; Chronic myeloid leukemia (CML); Acute myeloid leukemia (AML); Acute lymphoid leukemia (ALL); Myeloproliferative syndrome (MPS); Splice variant
类别
资金
- Mildred Scheel Stiftung fur Krebsforschung, Germany
- Deutsche Forschungsgemeinschaft (DFG)
- Universitatsklinikum Essen, Essen, Germany
Gfi1b is a transcriptional repressor that is essential for erythroid cells and megakaryocytes, but is also expressed in hematopoietic stem cells and early myeloid progenitors. The chromosomal localization of the Gfi1b gene at 9q34 and its functional homology with the proto-oncogene Gfi1 were suggestive for a role of Gfi1b in malignant transformation and myeloid leukemia. We show here that the expression of Gfi1b is strongly elevated in CML and AML patients compared to normal healthy controls and that imatinib, a drug widely used to treat CML, further enhances Gfi1b expression in patients even after remission. Our data suggest that Gfi1b may be an important factor to establish or maintain myeloid leukemia and myeloproliferative diseases and that, high expression levels of Gfi1b might be associated with the emergence of Philadelphia chromosome negative myeloid malignancies after imatinib withdrawal or after the development of imatinib resistance.
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