ReviewAmerican journal of hematology2016
A three-signal model of T-cell lymphoma pathogenesis.
Review in American journal of hematology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 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
54 citing papers in PubMed, 73 citations in OpenAlex.
- A single center phase II study of ixazomib in patients with relapsed or refractory cutaneous or peripheral T-cell lymphomas.American journal of hematology · 2017Trial
- Trial
- Functional genomics and proteomics identify Folate Carrier SLC19A1 as a predictor of pralatrexate sensitivity in diverse T-cell lymphoma models.Molecular cancer therapeutics · 2026Article
- CDK9 is a dependency in GATA-3 driven and MCL-1 independent T-cell Lymphomas.Blood cancer journal · 2025Article
- Integrating functional genomics and proteomics identifies Folate Carrier SLC19A1 as a predictor of pralatrexate sensitivity in T-cell lymphoma.bioRxiv : the preprint server for biology · 2025Article
- Mycosis Fungoides, Sézary Syndrome, and Cutaneous B-Cell Lymphomas: 2025 Update on Diagnosis, Risk-Stratification, and Management.American journal of hematology · 2025Review
- Ceramide signaling in immunity: a molecular perspective.Lipids in health and disease · 2025Review
- Article
- Multi-Omic Data Integration Suggests Putative Microbial Drivers of Aetiopathogenesis in Mycosis Fungoides.Cancers · 2024Article
- Successful anti-tumor effects with two novel bifunctional chemotherapeutic compounds that combine a LAT1 substrate with cytotoxic moieties in aggressive T-cell lymphomas.Leukemia research reports · 2024Article
- The OX40-TRAF6 axis promotes CTLA-4 degradation to augment antitumor CD8Cellular & molecular immunology · 2023Article
- SOHO State of the Art Updates and Next Questions | New Pathways and New Targets in PTCL: Staying on Target.Clinical lymphoma, myeloma & leukemia · 2023Review
- T-Cell Prolymphocytic Leukemia: Diagnosis, Pathogenesis, and Treatment.International journal of molecular sciences · 2023Review
- ITK degradation to block T cell receptor signaling and overcome therapeutic resistance in T cell lymphomas.Cell chemical biology · 2023Article
- Cutaneous Lymphoma and Antibody-Directed Therapies.Antibodies (Basel, Switzerland) · 2023Review
- Challenges in nodal peripheral T-cell lymphomas: from biological advances to clinical applicability.Frontiers in oncology · 2023Review
- Role of cytokine in malignant T-cell metabolism and subsequent alternation in T-cell tumor microenvironment.Frontiers in oncology · 2023Review
- Cutaneous T-cell lymphomas: 2023 update on diagnosis, risk-stratification, and management.American journal of hematology · 2023Article
- PTCL, NOS: An update on classification, risk-stratification, and treatment.Frontiers in oncology · 2023Review
- Targeting Lymphoma-associated Macrophage Expansion via CSF1R/JAK Inhibition is a Therapeutic Vulnerability in Peripheral T-cell Lymphomas.Cancer research communications · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
T-cell lymphoma pathogenesis and classification have, until recently, remained enigmatic. Recently performed whole-exome sequencing and gene-expression profiling studies have significant implications for their classification and treatment. Recurrent genetic modifications in antigen ("signal 1"), costimulatory ("signal 2"), or cytokine receptors ("signal 3"), and the tyrosine kinases and other signaling proteins they activate, have emerged as important therapeutic targets in these lymphomas. Many of these genetic modifications do not function in a cell-autonomous manner, but require the provision of ligand(s) by constituents of the tumor microenvironment, further supporting the long-appreciated view that these lymphomas are dependent upon and driven by their microenvironment. Therefore, the seemingly disparate fields of genomics and immunology are converging. A unifying "3 signal model" for T-cell lymphoma pathogenesis that integrates these findings will be presented, and its therapeutic implications briefly reviewed.
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.