ArticleInternational journal of hematology2009
Growth factor independent 1b (Gfi1b) and a new splice variant of Gfi1b are highly expressed in patients with acute and chronic leukemia.
Article in International journal of hematology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
29 citing papers in PubMed, 50 citations in OpenAlex.
- Significance of expression of ITGA5 and its splice variants in acute myeloid leukemia: a report from the Children's Oncology Group.American journal of hematology · 2013Trial
- GFI1B mutations define an emerging form of inherited thrombocytopenia: insights from a case report and literature review.Annals of hematology · 2026Review
- Alternative splicing events show high prognostic values and indicate potential core genes in acute myeloid leukemia.Clinical and experimental medicine · 2026Article
- Article
- Dysregulation of oncogenic factors by GFI1B p32: investigation of a novelHaematologica · 2022Article
- Splicing Anomalies in Myeloproliferative Neoplasms: Paving the Way for New Therapeutic Venues.Cancers · 2020Review
- Epigenetic Regulation of Gfi1 in Endocrine-Related Cancers: a Role Regulating Tumor Growth.International journal of molecular sciences · 2020Article
- Impact of mutations in DNA methylation modification genes on genome-wide methylation landscapes and downstream gene activations in pan-cancer.BMC medical genomics · 2020Article
- Multifaceted Actions of GFI1 and GFI1B in Hematopoietic Stem Cell Self-Renewal and Lineage Commitment.Frontiers in genetics · 2020Review
- Growth Factor Independence 1B-Mediated Transcriptional Repression and Lineage Allocation Require Lysine-Specific Demethylase 1-Dependent Recruitment of the BHC Complex.Molecular and cellular biology · 2019Article
- Targeting the GFI1/1B-CoREST Complex in Acute Myeloid Leukemia.Frontiers in oncology · 2019Review
- Gfi1b: a key player in the genesis and maintenance of acute myeloid leukemia and myelodysplastic syndrome.Haematologica · 2018Article
- Prognostic significance of high GFI1 expression in AML of normal karyotype and its association with a FLT3-ITD signature.Scientific reports · 2017Article
- Transcription Factor GFI1B in Health and Disease.Frontiers in oncology · 2017Review
- Whole-Exome Sequencing Identifies Loci Associated with Blood Cell Traits and Reveals a Role for Alternative GFI1B Splice Variants in Human Hematopoiesis.American journal of human genetics · 2016Article
- Cooperative Stimulation of Megakaryocytic Differentiation by Gfi1b Gene Targets Kindlin3 and Talin1.PloS one · 2016Article
- Reciprocal regulation of alternative lineages by Rgs18 and its transcriptional repressor Gfi1b.Journal of cell science · 2016Article
- KDM1 class flavin-dependent protein lysine demethylases.Biopolymers · 2015Review
- RNA-Seq analysis identifies aberrant RNA splicing of TRIP12 in acute myeloid leukemia patients at remission.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014Article
- Transcriptional diversity during lineage commitment of human blood progenitors.Science (New York, N.Y.) · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.