ArticleLeukemia2017
Sensitizing acute myeloid leukemia cells to induced differentiation by inhibiting the RIP1/RIP3 pathway.
Article in Leukemia, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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
33 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.
- Advances in the Regulation of Hematopoietic Homeostasis by Programmed Cell Death Under Radiation Conditions.Stem cell reviews and reports · 2025Pooled it
- Inflammation as a central driver in AML pathogenesis and therapy resistance.Science China. Life sciences · 2026Review
- Pandora's Box of AML: HowBiomedicines · 2025Review
- Targeting cell death pathways in acute myeloid leukemia: Molecular mechanisms and clinical implications (Review).Oncology reports · 2025Review
- Mechanism and role of regulated cell death in tumor immunity and immunotherapy.Cancer communications (London, England) · 2025Review
- Programmed cell death regulates hematopoietic cell homeostasis under radiation conditions.Stem cell research & therapy · 2025Article
- Overexpression and oncogenic role of RIPK3 in acute myeloid leukemia associated with specific subtypes and treatment outcome.BMC cancer · 2025Article
- Identification of PANoptosis-based signature for predicting the prognosis and immunotherapy response in AML.Heliyon · 2024Article
- The dual role of FSP1 in programmed cell death: resisting ferroptosis in the cell membrane and promoting necroptosis in the nucleus of THP-1 cells.Molecular medicine (Cambridge, Mass.) · 2024Article
- Identification of a novel monocyte/macrophage-related gene signature for predicting survival and immune response in acute myeloid leukemia.Scientific reports · 2024Article
- Deregulation of New Cell Death Mechanisms in Leukemia.Cancers · 2024Review
- Plasma membrane repair empowers the necrotic survivors as innate immune modulators.Seminars in cell & developmental biology · 2024Review
- Distinct roles of hematopoietic cytokines in the regulation of leukemia stem cells in murine MLL-AF9 leukemia.Stem cell reports · 2024Article
- The anti-leukemia activity and mechanisms of shikonin: a mini review.Frontiers in pharmacology · 2023Review
- Targeting regulated cell death pathways in acute myeloid leukemia.Cancer drug resistance (Alhambra, Calif.) · 2023Review
- RIP kinases and necroptosis in aging and aging-related diseases.Life medicine · 2022Review
- Ripk3 signaling regulates HSCs during stress and represses radiation-induced leukemia in mice.Stem cell reports · 2022Article
- Review
- RIP1-dependent Apoptosis and Differentiation Regulated by Skp2 and Akt/GSK3β in Acute Myeloid Leukemia.International journal of medical sciences · 2022Article
- RIPK3 signaling and its role in the pathogenesis of cancers.Cellular and molecular life sciences : CMLS · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
24 authors at 6 institutions in 2 countries.
Funding
Abstract
Tumor necrosis factor-α (TNF-α)-induced RIP1/RIP3 (receptor-interacting protein kinase 1/receptor-interacting protein kinase 3)-mediated necroptosis has been proposed as an alternative strategy for treating apoptosis-resistant leukemia. However, we found that most acute myeloid leukemia (AML) cells, especially M4 and M5 subtypes, produce TNF and show basal level activation of RIP1/RIP3/MLKL signaling, yet do not undergo necroptosis. TNF, through RIP1/RIP3 signaling, prevents degradation of SOCS1, a key negative regulator of interferon-γ (IFN-γ) signaling. Using both pharmacologic and genetic assays, we show here that inactivation of RIP1/RIP3 resulted in reduction of SOCS1 protein levels and partial differentiation of AML cells. AML cells with inactivated RIP1/RIP3 signaling show increased sensitivity to IFN-γ-induced differentiation. RIP1/RIP3 inactivation combined with IFN-γ treatment significantly attenuated the clonogenic capacity of both primary AML cells and AML cell lines. This combination treatment also compromised the leukemogenic ability of murine AML cells in vivo. Our studies suggest that inhibition of RIP1/RIP3-mediated necroptotic signaling might be a novel strategy for the treatment of AML when combined with other differentiation inducers.
Indexed as
Identifiers
What OpenQuestion holds
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.