ArticleLeukemia2016
GFI1 as a novel prognostic and therapeutic factor for AML/MDS.
Article in Leukemia, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
34 citing papers in PubMed, 1 synthesis or guideline pooled it, 46 citations in OpenAlex.
- Schizophrenia is associated with altered DNA methylation variance.Molecular psychiatry · 2025Pooled it
- Discovery of BEND4 as a novel single-gene prognostic marker and therapeutic target for adverse AML.NPJ precision oncology · 2026Article
- Tobacco Smoke Exposure From Prenatal To Adolescent Periods Drives IBD Pathogenesis: Dynamic DNA Methylation Signatures Across Lifespan Stages.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- ELK1 promotes the progress of myeloid leukemia by hindering the differentiation of neutrophils.Experimental hematology & oncology · 2026Article
- Impact of Acute Myeloid Leukemia Cells on the Metabolic Function of Bone Marrow Mesenchymal Stem Cells.International journal of molecular sciences · 2025Article
- Germline Single-Nucleotide PolymorphismBiomedicines · 2025Article
- Evaluation of HOTAIRM1, miR-196b, and HOXA9 as Oncogenic Markers in Patients with Acute Myeloblastic Leukemia.Iranian journal of pathology · 2025Article
- The prognostic and therapeutic potential of HO-1 in leukemia and MDS.Cell communication and signaling : CCS · 2023Review
- Dose-dependent effect of GFI1 expression in the reconstitution and the differentiation capacity of HSCs.Frontiers in cell and developmental biology · 2023Article
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- Epigenetic Crosstalk between Malignant Plasma Cells and the Tumour Microenvironment in Multiple Myeloma.Cancers · 2022Review
- GFI1 Cooperates with IKZF1/IKAROS to Activate Gene Expression in T-cell Acute Lymphoblastic Leukemia.Molecular cancer research : MCR · 2022Article
- Presence of theFrontiers in oncology · 2022Article
- Curcumin as an Epigenetic Therapeutic Agent in Myelodysplastic Syndromes (MDS).International journal of molecular sciences · 2021Article
- Review
- Superior efficacy of co-targeting GFI1/KDM1A and BRD4 against AML and post-MPN secondary AML cells.Blood cancer journal · 2021Article
- A PML/RARα direct target atlas redefines transcriptional deregulation in acute promyelocytic leukemia.Blood · 2021Article
- IGFBP7 activates retinoid acid-induced responses in acute myeloid leukemia stem and progenitor cells.Blood advances · 2020Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
27 authors at 7 institutions in 3 countries.
Funding
Abstract
Genetic and epigenetic aberrations contribute to the initiation and progression of acute myeloid leukemia (AML). GFI1, a zinc-finger transcriptional repressor, exerts its function by recruiting histone deacetylases to target genes. We present data that low expression of GFI1 is associated with an inferior prognosis of AML patients. To elucidate the mechanism behind this, we generated a humanized mouse strain with reduced GFI1 expression (GFI1-KD). Here we show that AML development induced by onco-fusion proteins such as MLL-AF9 or NUP98-HOXD13 is accelerated in mice with low human GFI1 expression. Leukemic cells from animals that express low levels of GFI1 show increased H3K9 acetylation compared to leukemic cells from mice with normal human GFI1 expression, resulting in the upregulation of genes involved in leukemogenesis. We investigated a new epigenetic therapy approach for this subgroup of AML patients. We could show that AML blasts from GFI1-KD mice and from AML patients with low GFI1 levels were more sensitive to treatment with histone acetyltransferase inhibitors than cells with normal GFI1 expression levels. We suggest therefore that GFI1 has a dose-dependent role in AML progression and development. GFI1 levels are involved in epigenetic regulation, which could open new therapeutic approaches for AML patients.
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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.