Submit Data |  Help |  Video Tutorials |  News |  Publications |  FTP Download |  REST API |  Citing RGD |  Contact   

Growth factor independent 1b (Gfi1b) and a new splice variant of Gfi1b are highly expressed in patients with acute and chronic leukemia.

Authors: Vassen, L  Khandanpour, C  Ebeling, P  Van der Reijden, BA  Jansen, JH  Mahlmann, S  Duhrsen, U  Moroy, T 
Citation: Vassen L, etal., Int J Hematol. 2009 May;89(4):422-30. doi: 10.1007/s12185-009-0286-5. Epub 2009 Apr 10.
Pubmed: (View Article at PubMed) PMID:19360458
DOI: Full-text: DOI:10.1007/s12185-009-0286-5

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.


Disease Annotations
Objects Annotated

Additional Information

CRRD Object Information
CRRD ID: 11040460
Created: 2016-03-08
Species: All species
Last Modified: 2016-03-08
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.