ReviewSignal transduction and targeted therapy2026
Humoral immunity in cancer.
Review in Signal transduction and targeted therapy, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- B Cells and Tumor Immunometabolism: Emerging Insights into Immune Regulation and Therapeutic Resistance.Antibodies (Basel, Switzerland) · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Humoral immunity driven by B cells, plasma cells, and antibodies has emerged as a major determinant of tumor control, immune escape, and therapeutic response. Across solid tumors, mature tertiary lymphoid structures (TLS) with high endothelial venules, follicular dendritic-cell networks, and T follicular helper cell niches support germinal-center-like reactions, B-cell receptor selection, somatic hypermutation, class-switch recombination, antigen presentation, and local humoral memory. However, B-lineage responses are not uniformly protective. Regulatory B cells, IgA- or IgG4-skewed plasma cells, inhibitory Fc-receptor signaling, chronic immune complexes, and tumor-imposed metabolic stress can suppress cytotoxic immunity and reprogram myeloid compartments. This review synthesizes the mechanisms that determine whether humoral immunity is antitumor or protumor, including TLS maturity, B-cell and plasma-cell states, antibody subclass and tissue geography, Fc glycosylation, Fc-receptor balance, complement context, immunometabolic adaptation, and spatial organization. We also discuss how single-cell, B-cell receptor repertoire, spatial transcriptomic, and spatial proteomic approaches can resolve antigen-driven B-cell selection and distinguish TLS-organized effector niches from diffuse regulatory infiltrates. Finally, we map current and emerging therapeutic strategies, from approved B-cell and antibody-directed agents in hematologic malignancies to TLS-inducing, Fc-engineering, vaccine, and isotype-modulating approaches in solid tumors, and we propose biomarker-guided guardrails for clinical translation. These guardrails are intended to preserve protective TLS-linked immunity while selectively targeting suppressive humoral programs.
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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.