ReviewBlood2017
Signaling pathways and immune evasion mechanisms in classical Hodgkin lymphoma.
Review in Blood, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 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
46 citing papers in PubMed.
- Proteomic Profiles and Biological Processes of Relapsed vs. Non-Relapsed Pediatric Hodgkin Lymphoma.International journal of molecular sciences · 2020Trial
- Article
- Genetic risk and immune dysregulation of classic Hodgkin lymphoma transformation of chronic lymphocytic leukemia/small lymphocytic lymphoma: a multicentric study.medRxiv : the preprint server for health sciences · 2026Article
- Integrating Flow Cytometry in the Diagnostic Work of HIV-Associated Hodgkin's Lymphomas.Journal of cellular and molecular medicine · 2026Review
- Predictors of sensitivity to immune therapies in classic Hodgkin lymphoma.Blood neoplasia · 2026Review
- Anti-TIM-3 antibody TQB2618 in combination with penpulimab in relapsed or refractory classic Hodgkin lymphoma previously treated with PD-1/PD-L1 therapy: a multicenter, open-label, single-arm, phase Ib clinical trial.Journal for immunotherapy of cancer · 2026Article
- Outcome of Autologous Stem Cell Transplant in Relapsed/Refractory Hodgkin Lymphoma - A Single Center Study.Journal of cancer & allied specialties · 2026Article
- Evolution of therapeutic paradigms in Hodgkin lymphoma: from "cure-oriented" to "functional cure".Frontiers in oncology · 2026Review
- Spatial Analysis of the Tumor Microenvironment in Diffuse Large B-cell Lymphoma Reveals Clinically Relevant Cell Interactions and Recurrent Cellular Neighborhoods.Cancer immunology research · 2025Article
- Viral oncogenesis in cancer: from mechanisms to therapeutics.Signal transduction and targeted therapy · 2025Review
- Review
- PRMT3 drives PD-L1-mediated immune escape through activating PDHK1-regulated glycolysis in hepatocellular carcinoma.Cell death & disease · 2025Article
- Molecular profiling of cell-free DNA from classic Hodgkin lymphoma patients identifies potential prognostic clusters and corresponds with disease dynamics.Annals of hematology · 2025Article
- Article
- Immune checkpoint inhibitors in advanced and relapsed/refractory Hodgkin lymphoma: current applications and future prospects.Frontiers in oncology · 2024Review
- Unraveling the Immune Microenvironment in Classic Hodgkin Lymphoma: Prognostic and Therapeutic Implications.Biology · 2023Review
- Genetic lesions and targeted therapy in Hodgkin lymphoma.Therapeutic advances in hematology · 2023Review
- Longitudinal Body Composition Changes Detected by [Cancers · 2022Article
- Ferritin, sex, and the wildfire of inflammation in Hodgkin lymphoma.Leukemia & lymphoma · 2022Article
- Clinical Impact of Immune Cells and Their Spatial Interactions in Diffuse Large B-Cell Lymphoma Microenvironment.Clinical cancer research : an official journal of the American Association for Cancer Research · 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
2 authors.
Funding
Abstract
Classical Hodgkin lymphoma (cHL) is an unusual B-cell-derived malignancy in which rare malignant Hodgkin and Reed-Sternberg (HRS) cells are surrounded by an extensive but ineffective inflammatory/immune cell infiltrate. This striking feature suggests that malignant HRS cells escape immunosurveillance and interact with immune cells in the cancer microenvironment for survival and growth. We previously found that cHLs have a genetic basis for immune evasion: near-uniform copy number alterations of chromosome 9p24.1 and the associated PD-1 ligand loci, CD274/PD-L1 and PDCD1LG2/PD-L2, and copy number-dependent increased expression of these ligands. HRS cells expressing PD-1 ligands are thought to engage PD-1 receptor-positive immune effectors in the tumor microenvironment and induce PD-1 signaling and associated immune evasion. The genetic bases of enhanced PD-1 signaling in cHL make these tumors uniquely sensitive to PD-1 blockade.
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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.