ReviewBlood2024
The role of the MDM2/p53 axis in antitumor immune responses.
Review in Blood, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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, 50 citations in OpenAlex.
- E3 Ubiquitin Ligase MDM2 Promotes Growth and CD8Journal of gastroenterology and hepatology · 2026Article
- MYC in Oncogenesis and Therapeutic Implications.MedComm · 2026Review
- FBXO5 regulates RPL23A to promote MDM2-mediated p53 degradation and facilitate malignant progression of breast cancer.Breast cancer research : BCR · 2026Article
- A diabetes-induced change of MDM2 SNP309T→G contributes to aberrant retinal angiogenesis.Diabetologia · 2026Article
- p53: from understanding its structure to advances in therapeutic targeting.Signal transduction and targeted therapy · 2026Review
- Isothiocyanate-mediated cyclization of phage-displayed peptides enables discovery of macrocyclic binders.Science advances · 2026Article
- Molecular Characteristics, Circularization Mechanism, and Potential Functions of circRNA-0172.Genes · 2025Article
- MDM2 promotes CELF6 ubiquitination-dependent degradation to promote neuroblastoma cell proliferation.Cell death & disease · 2025Article
- Exploring the mechanisms of cinobufotalin in ovarian cancer treatment: An integrated approach combining network pharmacology, molecular docking and RNA Sequencing.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Review
- Thyroid differentiation score-related genes and prognostic model for thyroid cancer.Translational cancer research · 2025Article
- Correlation ofCurrent oncology (Toronto, Ont.) · 2025Article
- Lipid Droplet-Organized MDM2-Mediated P53 Degradation: A Metabolic Switch Governing Diet-Driven Tumor Progression.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- CAR-T cell therapy for cancer: current challenges and future directions.Signal transduction and targeted therapy · 2025Review
- Bio-engineered microRNA-7 effectively interferes with the Akt3/p53 axis to suppress human non-small cell lung cancer.Cancer cell international · 2025Article
- Targeting PD-1 post-translational modifications for improving cancer immunotherapy.Cell insight · 2025Review
- TTLL4 mediates the PI3K/AKT/MDM2 pathway to promote hepatocellular carcinoma progression and predict patient prognosis.APL bioengineering · 2025Article
- Effect of deubiquitinases in head and neck squamous cell carcinoma (Review).Oncology letters · 2025Review
- Gelsolin's Protective Role in MASH through F-Actin Regulation and P53 Degradation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Skimmianine Modulates Tumor Proliferation and Immune Dynamics in Breast Cancer by Targeting PCNA and TNF-α.Pharmaceuticals (Basel, Switzerland) · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
abstractMouse double minute 2 homolog (MDM2) is a negative regulator of the tumor suppressor p53 and is often highly expressed in acute myeloid leukemia (AML) and other solid tumors. Inactivating mutations in TP53, the gene encoding p53, confers an unfavorable prognosis in AML and increases the risk for relapse after allogeneic hematopoietic cell transplantation. We review the concept that manipulation of MDM2 and p53 could enhance immunogenicity of AML and solid tumor cells. Additionally, we discuss the mechanisms by which MDM2 and p53 regulate the expression of major histocompatibility complex class I and II, transcription of double stranded RNA of endogenous retroviruses, responses of interferons, production of interleukin-15, and expression of tumor necrosis factor-related apoptosis-inducing ligand receptor 1 and 2 on malignant cells. The direct effects of MDM2 inhibition or MDM2 deletion in effector T cells are discussed in the context of cancer immunotherapy. The preclinical findings are connected to clinical studies using MDM2 inhibition to enhance antitumor immunity in patients. This review summarizes current evidence supporting the use of MDM2 inhibition to restore p53 as well as the direct effects of MDM2 inhibition on T cells as an emerging concept for combined antitumor immunotherapy against hematological malignancies and beyond.
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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.