ArticleThe Journal of clinical investigation2022
Tumor-associated antigen PRAME exhibits dualistic functions that are targetable in diffuse large B cell lymphoma.
Article in The Journal of clinical investigation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 22 citations in OpenAlex.
- Emergence of the cancer antigen PRAME as key player in epigenetic dysregulation and renal tumorigenesis.Cell death and differentiation · 2026Article
- Article
- Mutational profiling of HIV+ diffuse large B-cell lymphoma reveals distinct mutational features with evidence of genomic instability.AIDS (London, England) · 2026Article
- DNA hypomethylation-activated PRAME drives early-stage lung adenocarcinoma recurrence via ZNF740 and PI3K/AKT/mTOR signaling.Translational lung cancer research · 2026Article
- Shared PRAME epitopes are T-cell targets in NUT carcinoma.Journal for immunotherapy of cancer · 2026Article
- Characterization of the genomic landscape of canine diffuse large B-cell lymphoma reveals recurrent H3K27M mutations linked to progression-free survival.Scientific reports · 2025Article
- EZH2 inhibition enhances T cell immunotherapies by inducing lymphoma immunogenicity and improving T cell function.Cancer cell · 2025Article
- mRNA vaccines in tumor targeted therapy: mechanism, clinical application, and development trends.Biomarker research · 2024Review
- Comprehensive review of CRISPR-based gene editing: mechanisms, challenges, and applications in cancer therapy.Molecular cancer · 2024Review
- Targeting PRAME for acute myeloid leukemia therapy.Frontiers in immunology · 2024Review
- PRAME Expression: A Target for Cancer Immunotherapy and a Prognostic Factor in Uveal Melanoma.Investigative ophthalmology & visual science · 2023Article
- Review
- Transcriptome Analysis of Diffuse Large B-Cell Lymphoma Cells Inducibly Expressing MyD88 L265P Mutation Identifies Upregulated CD44, LGALS3, NFKBIZ, and BATF as Downstream Targets of Oncogenic NF-κB Signaling.International journal of molecular sciences · 2023Article
- The Immunology of DLBCL.Cancers · 2023Review
- Epigenetics in lymphocyte and lymphoma: EZH2 as an easy-to-access therapeutic target?International journal of hematology · 2022Article
- Genetic mechanism for the loss of PRAME in B cell lymphomas. Reply.The Journal of clinical investigation · 2022Article
- Genetic mechanism for the loss of PRAME in B cell lymphomas.The Journal of clinical investigation · 2022Article
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36 authors at 4 institutions in 3 countries.
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Abstract
PRAME is a prominent member of the cancer testis antigen family of proteins, which triggers autologous T cell-mediated immune responses. Integrative genomic analysis in diffuse large B cell lymphoma (DLBCL) uncovered recurrent and highly focal deletions of 22q11.22, including the PRAME gene, which were associated with poor outcome. PRAME-deleted tumors showed cytotoxic T cell immune escape and were associated with cold tumor microenvironments. In addition, PRAME downmodulation was strongly associated with somatic EZH2 Y641 mutations in DLBCL. In turn, PRC2-regulated genes were repressed in isogenic PRAME-KO lymphoma cell lines, and PRAME was found to directly interact with EZH2 as a negative regulator. EZH2 inhibition with EPZ-6438 abrogated these extrinsic and intrinsic effects, leading to PRAME expression and microenvironment restoration in vivo. Our data highlight multiple functions of PRAME during lymphomagenesis and provide a preclinical rationale for synergistic therapies combining epigenetic reprogramming with PRAME-targeted therapies.
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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.