ArticleNeuro-oncology2025
Distinct epigenetic and transcriptional profiles of Epstein-Barr virus-positive and negative primary CNS lymphomas.
Article in Neuro-oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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
12 citing papers in PubMed.
- Advances in molecular pathobiology of PCNSL - towards clinical implementation of novel diagnostics and therapeutics.Biomarker research · 2026Review
- Genetic orchestration of the primary central nervous system lymphoma microenvironment.Biomarker research · 2026Review
- Primary central nervous system lymphoma in the molecular era: genomic drivers, liquid biopsy, and targeted therapeutic strategies.Annals of hematology · 2026Review
- Article
- Time Is Key: Early Diagnosis of Post-Transplant Lymphoproliferative Disorder Presenting as Primary CNS Diffuse Large B-Cell Lymphoma.Current oncology (Toronto, Ont.) · 2026Article
- Unraveling the immune microenvironment in primary CNS lymphoma.Biomarker research · 2026Review
- Candidate MRI biomarkers for CD79B status in primary CNS lymphoma: an exploratory radiogenomic analysis of the UCSF-PCNSL cohort.Journal of neuro-oncology · 2026Article
- Article
- Patterns, risk factors and management of CD19-directed chimeric antigen receptor T-cell therapy failure in CNS lymphoma.Journal of hematology & oncology · 2026Article
- Acalabrutinib May Offer a New Therapeutic Approach for Consolidation and Maintenance of Primary CNS Lymphoma with Expression of MYD88 and CD79B Gene Variants: A Case Report and Literature Review of Primary CNS Lymphoma in the BTKi Era.International journal of molecular sciences · 2025Review
- Article
- Liver injury in sepsis: manifestations, mechanisms and emerging therapeutic strategies.Frontiers in immunology · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
19 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundEpstein-Barr virus (EBV)+ and EBV- primary CNS lymphomas (PCNSL) carry distinct mutational landscapes, but their transcriptional and epigenetic profiles have not been integrated and compared. This precludes further insights into pathobiology and molecular differences, relevant for classification and targeted therapy.
methodsTwenty-three EBV- and 15 EBV+ PCNSL, histologically classified as diffuse large B-cell lymphomas, were subjected to RNA-sequencing and EPIC methylation arrays. Unsupervised clustering analyses were performed. Differentially expressed and differentially methylated genes were identified and integrated.
resultsTwo distinct transcriptional clusters were found, which separated EBV- and EBV+ PCNSL (P < .0001). The EBV+ transcriptional signature contained genes (GPR15, FCER2/CD23, SLAMF1/CD150) closely regulated by EBV oncogenes in B cells. Pathway enrichment analysis uncovered enhanced B-cell receptor (BCR) and WNT/beta-catenin signaling in EBV- lymphomas, whereas Interleukin-10, NOTCH, and viral life cycle pathways were upregulated in EBV+ PCNSL. Correspondingly, BCR-associated SYK kinase activity was enriched in EBV- tumors while JAK2 was overrepresented in EBV+ PCNSL. Epigenetic profiling revealed reduced global promoter methylation in EBV+ PCNSL. Two methylation clusters were recognized, which separated EBV- and EBV+ PCNSL (P < .0001). Epigenetic profiles were distinct from 2,788 other brain tumor and nonmalignant reference samples. Promoter region hypermethylation of CD79B, a BCR subunit critical for sustained proliferation in EBV- disease, highly correlated (R = -0.7) with its transcriptional downregulation in EBV+ PCNSL.
conclusionsEBV+ and EBV- PCNSL harbor distinct transcriptional and epigenetic profiles, corroborating them as distinctive biological subtypes. Uncovered differences provide novel insights into their pathobiology, may guide molecular diagnostics and targeted therapies.
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.