ArticleCancer cell2013
Growth factor independence 1 antagonizes a p53-induced DNA damage response pathway in lymphoblastic leukemia.
Article in Cancer cell, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 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.
The trial behind it
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Who cites it
51 citing papers in PubMed, 73 citations in OpenAlex.
- Growth factor independence 1 ameliorates osteoarthritis by inhibiting chondrocyte ferroptosis via inactivation of MAPK signaling pathway.Journal of orthopaedic translation · 2025Article
- Bcl-xL is important for the antiapoptotic activity of Gfi1 and is upregulated by Gfi1 through hemgn.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- Germ line variant GFI1-36N affects DNA repair and sensitizes AML cells to DNA damage and repair therapy.Blood · 2023Article
- Article
- LSD1 inhibition modulates transcription factor networks in myeloid malignancies.Frontiers in oncology · 2023Review
- GFI1 Cooperates with IKZF1/IKAROS to Activate Gene Expression in T-cell Acute Lymphoblastic Leukemia.Molecular cancer research : MCR · 2022Article
- GFI1-Dependent Repression ofCancers · 2022Article
- Curcumin as an Epigenetic Therapeutic Agent in Myelodysplastic Syndromes (MDS).International journal of molecular sciences · 2021Article
- Epigenetic regulation in medulloblastoma pathogenesis revealed by genetically engineered mouse models.Cancer science · 2021Review
- 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
- Gfi1 upregulates c-Myc expression and promotes c-Myc-driven cell proliferation.Scientific reports · 2020Article
- Combined inhibition of JAK/STAT pathway and lysine-specific demethylase 1 as a therapeutic strategy in CSF3R/CEBPA mutant acute myeloid leukemia.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Deubiquitinase MYSM1 in the Hematopoietic System and beyond: A Current Review.International journal of molecular sciences · 2020Review
- Multifaceted Actions of GFI1 and GFI1B in Hematopoietic Stem Cell Self-Renewal and Lineage Commitment.Frontiers in genetics · 2020Review
- Article
- A novel regulatory circuit between p53 and GFI1 controls induction of apoptosis in T cells.Scientific reports · 2019Article
- Gfi1-Mediated Repression of c-Fos, Egr-1 and Egr-2, and Inhibition of ERK1/2 Signaling Contribute to the Role of Gfi1 in Granulopoiesis.Scientific reports · 2019Article
- Lsd1 as a therapeutic target in Gfi1-activated medulloblastoma.Nature communications · 2019Article
- Targeting the GFI1/1B-CoREST Complex in Acute Myeloid Leukemia.Frontiers in oncology · 2019Review
Corrections and comments
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Authors and funding
14 authors at 5 institutions in 4 countries.
Funding
Abstract
Most patients with acute lymphoblastic leukemia (ALL) fail current treatments highlighting the need for better therapies. Because oncogenic signaling activates a p53-dependent DNA damage response and apoptosis, leukemic cells must devise appropriate countermeasures. We show here that growth factor independence 1 (Gfi1) can serve such a function because Gfi1 ablation exacerbates p53 responses and lowers the threshold for p53-induced cell death. Specifically, Gfi1 restricts p53 activity and expression of proapoptotic p53 targets such as Bax, Noxa (Pmaip1), and Puma (Bbc3). Subsequently, Gfi1 ablation cures mice from leukemia and limits the expansion of primary human T-ALL xenografts in mice. This suggests that targeting Gfi1 could improve the prognosis of patients with T-ALL or other lymphoid leukemias.
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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.