This is a preview of subscription content, access via your institution
Relevant articles
Open Access articles citing this article.
-
Reduced expression but not deficiency of GFI1 causes a fatal myeloproliferative disease in mice
Leukemia Open Access 20 June 2018
-
Enforced GFI1 expression impedes human and murine leukemic cell growth
Scientific Reports Open Access 16 November 2017
Access options
Subscribe to this journal
Receive 12 print issues and online access
$259.00 per year
only $21.58 per issue
Buy this article
- Purchase on Springer Link
- Instant access to full article PDF
Prices may be subject to local taxes which are calculated during checkout
References
Lidonnici MR, Audia A, Soliera AR, Prisco M, Ferrari-Amorotti G, Waldron T et al. Expression of the transcriptional repressor Gfi-1 is regulated by C/EBPα and is involved in its proliferation and colony formation-inhibitory effects in p210BCR/ABL-expressing cells. Cancer Res 2010; 70: 7949–7959.
Soliera AR, Mariani SA, Audia A, Lidonnici MR, Addya S, Ferrari-Amorotti G et al. Gfi-1 inhibits proliferation and colony formation of p210BCR/ABL-expressing cells via transcriptional repression of STAT 5 and Mcl-1. Leukemia 2012; 26: 1555–1563.
Dvinge H, Bertone P . HTqPCR: high-throughput analysis and visualization of quantitative real-time PCR data in R. Bioinformatics 2009; 25: 3325–3326.
Livak KJ, Schmittgen TD . Analysis of relative gene expression data using real-time quantitative PCR and the 2(-Delta Delta C(T)) method. Methods 2001; 25: 402–408.
van der Meer LT, Jansen JH, van der Reijden BA . Gfi1 and Gfi1b: key regulators of hematopoiesis. Leukemia 2010; 24: 1834–1843.
Huang M, Hu Z, Chang W, Ou D, Zhou J, Zhang Y . The growth factor independence-1 (Gfi1) is overexpressed in chronic myelogenous leukemia. Acta Haematol 2010; 123: 1–5.
Marin D, Ibrahim AR, Lucas C, Gerrard G, Wang L, Szydlo RM et al. Assessment of BCR-ABL1 transcript levels at 3 months is the only requirement for predicting outcome for patients with chronic myeloid leukemia treated with tyrosine kinase inhibitors. J Clin Oncol. 2012; 30: 232–238.
White DL, Saunders VA, Quinn SR, Manley PW, Hughes TP . Imatinib increases the intracellular concentration of nilotinib, which may explain the observed synergy between these drugs. Blood 2007; 109: 3609–3610.
White DL, Dang P, Engler J, Frede A, Zrim S, Osborn M et al. Functional activity of the OCT-1 protein is predictive of long-term outcome in patients with chronic-phase chronic myeloid leukemia treated with imatinib. J Clin Oncol. 2010; 28: 2761–2767.
O’Hare T, Eide CA, Deininger MW . Bcr-Abl kinase domain mutations, drug resistance, and the road to a cure for chronic myeloid leukemia. Blood 2007; 110: 2242–2249.
Sokal JE, Cox EB, Baccarani M, Tura S, Gomez GA, Robertson JE et al. Prognostic discrimination in ‘good-risk’ chronic granulocytic leukemia. Blood 1984; 63: 789–799.
McWeeney SK, Pemberton LC, Loriaux MM, Vartanian K, Willis SG, Yochum G et al. A gene expression signature of CD34+ cells to predict major cytogenetic response in chronic-phase chronic myeloid leukemia patients treated with imatinib. Blood 2010; 115: 315–325.
Radich JP, Dai H, Mao M, Oehler V, Schelter J, Druker B et al. Gene expression changes associated with progression and response in chronic myeloid leukemia. Proc Natl Acad Sci USA 2006; 103: 2794–2799.
Horman SR, Velu CS, Chaubey A, Bourdeau T, Zhu J, Paul WE et al. Gfi1 integrates progenitor versus granulocytic transcriptional programming. Blood 2009; 113: 5466–5475.
Khandanpour C, Kosan C, Gaudreau MC, Duhrsen U, Hebert J, Zeng H et al. Growth factor independence 1 protects hematopoietic stem cells against apoptosis but also prevents the development of a myeloproliferative-like disease. Stem Cells 2011; 29: 376–385.
Yucel R, Karsunky H, Klein-Hitpass L, Moroy T . The transcriptional repressor Gfi1 affects development of early, uncommitted c-Kit+ T cell progenitors and CD4/CD8 lineage decision in the thymus. J Exp Med 2003; 197: 831–844.
Acknowledgements
DBW is supported by a PhD scholarship from the Leukemia Foundation of Australia. TPH is an NHMRC Practitioner Fellow. This project was funded by a Leukemia and Lymphoma Society (LLS) grant and a NHMRC project grant.
Author information
Authors and Affiliations
Corresponding author
Ethics declarations
Competing interests
The authors declare no conflict of interest.
Rights and permissions
About this article
Cite this article
Kok, C., Watkins, D., Leclercq, T. et al. Low GFI1 expression in white blood cells of CP–CML patients at diagnosis is strongly associated with subsequent blastic transformation. Leukemia 27, 1427–1430 (2013). https://doi.org/10.1038/leu.2013.47
Published:
Issue Date:
DOI: https://doi.org/10.1038/leu.2013.47
This article is cited by
-
Reduced expression but not deficiency of GFI1 causes a fatal myeloproliferative disease in mice
Leukemia (2019)
-
Enforced GFI1 expression impedes human and murine leukemic cell growth
Scientific Reports (2017)
-
GFI1 as a novel prognostic and therapeutic factor for AML/MDS
Leukemia (2016)
-
Sustained inhibition of STAT5, but not JAK2, is essential for TKI-induced cell death in chronic myeloid leukemia
Leukemia (2015)
-
Selecting the Best Frontline Treatment in Chronic Myeloid Leukemia
Current Hematologic Malignancy Reports (2015)