ReviewNature reviews. Cancer2018
Autoimmunity checkpoints as therapeutic targets in B cell malignancies.
Review in Nature reviews. Cancer, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
26 citing papers in PubMed.
- Genomic and transcriptomic profiling reveals distinct molecular subsets associated with outcomes in mantle cell lymphoma.The Journal of clinical investigation · 2022Trial
- Alternative oncogenic drivers and sensitivity to BTK inhibition in CRISPR/Cas gene-edited human DLBCL cell models.Blood neoplasia · 2026Article
- Common origins of autoimmune diseases and lymphoid malignancies.Trends in immunology · 2025Review
- The persistent inflammation in COPD: is autoimmunity the core mechanism?European respiratory review : an official journal of the European Respiratory Society · 2024Review
- Dependency of B-Cell Acute Lymphoblastic Leukemia and Multiple Myeloma Cell Lines on MEN1 Extends beyond MEN1-KMT2A Interaction.International journal of molecular sciences · 2023Article
- Activity of tafasitamab in combination with rituximab in subtypes of aggressive lymphoma.Frontiers in immunology · 2023Article
- Does IFITM3 link inflammation to tumorigenesis?BMB reports · 2022Review
- Integrative multi-omics and drug response profiling of childhood acute lymphoblastic leukemia cell lines.Nature communications · 2022Article
- Surface Proteomics Reveals CD72 as a Target forCancer discovery · 2021Article
- Targeted PI3K/AKT-hyperactivation induces cell death in chronic lymphocytic leukemia.Nature communications · 2021Article
- Developmental partitioning of SYK and ZAP70 prevents autoimmunity and cancer.Molecular cell · 2021Article
- A hotspot mutation in transcription factor IKZF3 drives B cell neoplasia via transcriptional dysregulation.Cancer cell · 2021Article
- Rituximab and obinutuzumab differentially hijack the B cell receptor and NOTCH1 signaling pathways.iScience · 2021Article
- Precursor B-ALL Cell Lines Differentially Respond to SYK Inhibition by Entospletinib.International journal of molecular sciences · 2021Article
- Mechanisms of B Cell Receptor Activation and Responses to B Cell Receptor Inhibitors in B Cell Malignancies.Cancers · 2020Review
- Physiological levels of the PTEN-PI3K-AKT axis activity are required for maintenance of Burkitt lymphoma.Leukemia · 2020Article
- Immunotherapy for the Treatment of Acute Lymphoblastic Leukemia.Current oncology reports · 2020Review
- The regulators of BCR signaling during B cell activation.Blood science (Baltimore, Md.) · 2019Review
- B cell checkpoints in autoimmune rheumatic diseases.Nature reviews. Rheumatology · 2019Review
- Metabolic gatekeepers to safeguard against autoimmunity and oncogenic B cell transformation.Nature reviews. Immunology · 2019Review
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.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Targeted therapy of cancer typically focuses on inhibitors (for example, tyrosine kinase inhibitors) that suppress oncogenic signalling below a minimum threshold required for survival and proliferation of cancer cells. B cell acute lymphoblastic leukaemia and B cell lymphomas originate from various stages of development of B cells, which, unlike other cell types, are under intense selective pressure. The vast majority of newly generated B cells are autoreactive and die by negative selection at autoimmunity checkpoints (AICs). Owing to ubiquitous encounters with self-antigen, autoreactive B cells are eliminated by the overwhelming signalling strength of their autoreactive B cell receptor (BCR). A series of recent findings suggests that, despite malignant transformation, AICs are fully functional in B cell malignancies. This Opinion article proposes targeted engagement of AICs as a previously unrecognized therapeutic opportunity to overcome drug resistance in B cell malignancies.
Indexed as
Identifiers
29302068What 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.