Trial reportBlood2016
TNFRSF14 aberrations in follicular lymphoma increase clinically significant allogeneic T-cell responses.
Trial report in Blood, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
21 citing papers in PubMed, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.
- Mutational landscape of marginal zone B-cell lymphomas of various origin: organotypic alterations and diagnostic potential for assignment of organ origin.Virchows Archiv : an international journal of pathology · 2022Pooled it
- Article
- Targeted plasma proteomics reveals a central role of upregulated TNFRSF proteins in HIV-associated stroke.Nature communications · 2026Article
- Genomic heterogeneity in primary cutaneous follicular center lymphomas reveals different clinicopathological subgroups.HemaSphere · 2026Article
- Exploring new drug treatment targets for immune related bone diseases using a multi omics joint analysis strategy.Scientific reports · 2025Article
- Multi-omic biomarkers associated with multiple sclerosis: from Mendelian randomization to drug prediction.Scientific reports · 2025Article
- Molecular Mechanisms in the Transformation from Indolent to Aggressive B Cell Malignancies.Cancers · 2025Review
- Identification of Plasma Protein Biomarkers and Drug Targets for Hematologic Malignancies by Proteome-wide Mendelian Randomization.Journal of Cancer · 2025Article
- Cross-talk between disulfidptosis and immune check point genes defines the tumor microenvironment for the prediction of prognosis and immunotherapies in glioblastoma.Scientific reports · 2024Article
- Non-invasive detection of lymphoma with circulating tumor DNA features and protein tumor markers.Frontiers in oncology · 2024Article
- Single-cell RNA Sequencing Reveals Novel Cellular Factors for Response to Immunosuppressive Therapy in Aplastic Anemia.HemaSphere · 2023Article
- Comprehensive assessment of cellular senescence in the tumor microenvironment.Briefings in bioinformatics · 2022Article
- The Tumor Microenvironment in Follicular Lymphoma: Its Pro-Malignancy Role with Therapeutic Potential.International journal of molecular sciences · 2021Review
- Pan-cancer investigation of CENPK gene: clinical significance and oncogenic immunology.American journal of translational research · 2021Article
- Detection of new drivers of frequent B-cell lymphoid neoplasms using an integrated analysis of whole genomes.PloS one · 2021Article
- Lymphoma Heterogeneity Unraveled by Single-Cell Transcriptomics.Frontiers in immunology · 2021Review
- T follicular helper cells in germinal center B cell selection and lymphomagenesis.Immunological reviews · 2020Review
- Natural Autoantibodies in Chronic Pulmonary Diseases.International journal of molecular sciences · 2020Review
- High TNFRSF14 and low BTLA are associated with poor prognosis in Follicular Lymphoma and in Diffuse Large B-cell Lymphoma transformation.Journal of clinical and experimental hematopathology : JCEH · 2019Article
- Herpesvirus Entry Mediator and Ocular Herpesvirus Infection: More than Meets the Eye.Journal of virology · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Donor T-cell immune responses can eradicate lymphomas after allogeneic hematopoietic stem cell transplantation (AHSCT), but can also damage healthy tissues resulting in harmful graft-versus-host disease (GVHD). Next-generation sequencing has recently identified many new genetic lesions in follicular lymphoma (FL). One such gene, tumor necrosis factor receptor superfamily 14 (TNFRSF14), abnormal in 40% of FL patients, encodes the herpes virus entry mediator (HVEM) which limits T-cell activation via ligation of the B- and T-lymphocyte attenuator. As lymphoma B cells can act as antigen-presenting cells, we hypothesized that TNFRSF14 aberrations that reduce HVEM expression could alter the capacity of FL B cells to stimulate allogeneic T-cell responses and impact the outcome of AHSCT. In an in vitro model of alloreactivity, human lymphoma B cells with TNFRSF14 aberrations had reduced HVEM expression and greater alloantigen-presenting capacity than wild-type lymphoma B cells. The increased immune-stimulatory capacity of lymphoma B cells with TNFRSF14 aberrations had clinical relevance, associating with higher incidence of acute GVHD in patients undergoing AHSCT. FL patients with TNFRSF14 aberrations may benefit from more aggressive immunosuppression to reduce harmful GVHD after transplantation. Importantly, this study is the first to demonstrate the impact of an acquired genetic lesion on the capacity of tumor cells to stimulate allogeneic T-cell immune responses which may have wider consequences for adoptive immunotherapy strategies.
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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.