ArticleNature neuroscience2020
Tumor necrosis factor overcomes immune evasion in p53-mutant medulloblastoma.
Article in Nature neuroscience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 31 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
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
31 citing papers in PubMed, 41 citations in OpenAlex.
- A novel Pyroptosis-related long non-coding RNA signature for predicting the prognosis and immune landscape of head and neck squamous cell carcinoma.Cancer medicine · 2022Trial
- Feedback regulation of VISTA and Treg by TNF-α controls T cell responses in drug allergy.Allergy · 2025Article
- Integrating single cell and bulk RNA sequencing data identifies RBM17 as a novel response biomarker for immunotherapy in bladder cancer.Virchows Archiv : an international journal of pathology · 2024Article
- Cancer marker TNFRSF1A: From single‑cell heterogeneity of renal cell carcinoma to functional validation.Oncology letters · 2024Article
- Targeting pediatric cancers via T-cell recognition of the monomorphic MHC class I-related protein MR1.Journal for immunotherapy of cancer · 2024Article
- Review
- Distinct immune escape and microenvironment between RG-like and pri-OPC-like glioma revealed by single-cell RNA-seq analysis.Frontiers of medicine · 2024Article
- Strategies to overcome low MHC-I expression in paediatric and adult tumours.Immunotherapy advances · 2024Review
- Global metabolomics study on the pathogenesis of pediatric medulloblastoma via UPLC- Q/E-MS/MS.PloS one · 2023Article
- Targeting mutant p53 stabilization for cancer therapy.Frontiers in pharmacology · 2023Review
- Tumor Necrosis Factor-Mediators of inflammation · 2023Article
- Epigenetic modulation of neuroblastoma enhances T cell and NK cell immunogenicity by inducing a tumor-cell lineage switch.Journal for immunotherapy of cancer · 2022Article
- Mutant p53 in cancer: from molecular mechanism to therapeutic modulation.Cell death & disease · 2022Review
- Nuclear factor kappa B signaling within the rat nucleus accumbens core sex-dependently regulates cue-induced cocaine seeking and matrix metalloproteinase-9 expression.Brain, behavior, and immunity · 2022Article
- Review
- Novel necroptosis-related gene signature for predicting the prognosis of pancreatic adenocarcinoma.Aging · 2022Article
- FABP4 activates the JAK2/STAT2 pathway via Rap1a in the homocysteine-induced macrophage inflammatory response in ApoELaboratory investigation; a journal of technical methods and pathology · 2022Article
- Hypothesis: Mutations and Immunosurveillance in Obesity-Associated Colorectal Cancer.Journal of Cancer · 2022Article
- Recent Advances in Pediatric Cancer Research.Cancer research · 2021Review
- Immunotherapy in Medulloblastoma: Current State of Research, Challenges, and Future Perspectives.Cancers · 2021Review
Corrections and comments
- Retraction · 2021-12-14Results Not Reproducible · Unreliable Data · Unreliable Results and/or Conclusions ·
- Retracted
Authors and funding
40 authors at 11 institutions in 4 countries.
Funding
Abstract
Many immunotherapies act by enhancing the ability of cytotoxic T cells to kill tumor cells. Killing depends on T cell recognition of antigens presented by class I major histocompatibility complex (MHC-I) proteins on tumor cells. In this study, we showed that medulloblastomas lacking the p53 tumor suppressor do not express surface MHC-I and are therefore resistant to immune rejection. Mechanistically, this is because p53 regulates expression of the peptide transporter Tap1 and the aminopeptidase Erap1, which are required for MHC-I trafficking to the cell surface. In vitro, tumor necrosis factor (TNF) or lymphotoxin-β receptor agonist can rescue expression of Erap1, Tap1 and MHC-I on p53-mutant tumor cells. In vivo, low doses of TNF prolong survival and synergize with immune checkpoint inhibitors to promote tumor rejection. These studies identified p53 as a key regulator of immune evasion and suggest that TNF could be used to enhance sensitivity of tumors to immunotherapy.
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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.