ArticleLeukemia2016
Recurrent activating mutations of CD28 in peripheral T-cell lymphomas.
Article in Leukemia, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 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.
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Who cites it
86 citing papers in PubMed, 126 citations in OpenAlex.
- Trial
- Targeting CD28 on T lineage malignancies with chimeric antigen receptor T cells.Nature communications · 2026Article
- From molecular pathogenesis to novel Therapeutic approaches - a review of recent advances in the treatment of peripheral T cell Lymphomas.Biomarker research · 2026Review
- Regulation of immune checkpoint molecules in cancer immune evasion and therapy.Nature reviews. Cancer · 2026Review
- T cell lymphomas: cancers of aberrant immune synapse signalling.Nature reviews. Immunology · 2026Review
- CD40LG/CD28-Mediated Rho GTPase Signaling Drives Survival and Chemoresistance in Non-ETP T-ALL.International journal of molecular sciences · 2026Article
- Genome-epigenome crosstalk in T-cell lymphomas: from maps to mechanisms.International journal of hematology · 2026Review
- Unraveling the many faces of angioimmunoblastic T-cell lymphoma: clinical, pathological, and molecular heterogeneity.Annals of hematology · 2026Review
- Insights into Nodal T-Follicular Helper Cell lymphomas and Peripheral T-Cell Lymphomas, Not Otherwise Specified, in Slovenian Patients: Mutational Landscape, Clinicopathological Characteristics, and Outcomes.Annals of hematology · 2025Article
- CDK9 is a dependency in GATA-3 driven and MCL-1 independent T-cell Lymphomas.Blood cancer journal · 2025Article
- Integrative Genomic and Transcriptomic Analysis Reveals Targetable Vulnerabilities in Angioimmunoblastic T-Cell Lymphoma.American journal of hematology · 2025Article
- Review
- Binding of RHOA G17V to p300 enhances its HAT activity: a new mechanism of epigenetic deregulation in TFH lymphoma.Blood advances · 2025Article
- Discrete genetic subtypes and tumor microenvironment signatures correlate with peripheral T-cell lymphoma outcomes.Leukemia · 2025Article
- Advances in peripheral T cell lymphomas: pathogenesis, genetic landscapes and emerging therapeutic targets.Histopathology · 2025Review
- Review
- TP53 and KMT2D mutations associated with worse prognosis in peripheral T-cell lymphomas.Cancer medicine · 2024Article
- BACH2-mediated CD28 and CD40LG axes contribute to pathogenesis and progression of T-cell lymphoblastic leukemia.Cell death & disease · 2024Article
- Advances in the pathogenesis and therapeutic strategies of angioimmunoblastic T-cell lymphoma.Clinical and experimental medicine · 2023Review
- Pathobiology of nodal peripheral T-cell lymphomas: current understanding and future directions.Haematologica · 2023Review
26 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
28 authors at 9 institutions in 6 countries.
Funding
Abstract
Peripheral T-cell lymphomas (PTCLs) comprise a heterogeneous group of mature T-cell neoplasms with a poor prognosis. Recently, mutations in TET2 and other epigenetic modifiers as well as RHOA have been identified in these diseases, particularly in angioimmunoblastic T-cell lymphoma (AITL). CD28 is the major co-stimulatory receptor in T cells which, upon binding ligand, induces sustained T-cell proliferation and cytokine production when combined with T-cell receptor stimulation. We have identified recurrent mutations in CD28 in PTCLs. Two residues-D124 and T195-were recurrently mutated in 11.3% of cases of AITL and in one case of PTCL, not otherwise specified (PTCL-NOS). Surface plasmon resonance analysis of mutations at these residues with predicted differential partner interactions showed increased affinity for ligand CD86 (residue D124) and increased affinity for intracellular adaptor proteins GRB2 and GADS/GRAP2 (residue T195). Molecular modeling studies on each of these mutations suggested how these mutants result in increased affinities. We found increased transcription of the CD28-responsive genes CD226 and TNFA in cells expressing the T195P mutant in response to CD3 and CD86 co-stimulation and increased downstream activation of NF-κB by both D124V and T195P mutants, suggesting a potential therapeutic target in CD28-mutated PTCLs.
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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.