ArticleCancer research2026
Base Editing of TIGIT Reprograms CD155 Signaling in Natural Killer Cells to Enhance Cancer Immunotherapy Efficacy.
Article in Cancer research, 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.
- Endogenous reprogramming of NK cell activation signal via base editing.Molecular therapy. Oncology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors.
Funding
Abstract
NK cells hold great promise for cancer immunotherapy owing to their intrinsic capacity to recognize and eliminate malignant cells. Nevertheless, broad clinical deployment is hindered by NK-cell properties like poor expansion and refractoriness to genetic modification, as well as by tumor immune-evasion mechanisms. In this study, we applied base-editing technology to precisely modify signal transduction in primary human NK cells, which achieved a high editing efficiency of the T-cell immunoreceptor with Ig and ITIM domains (TIGIT) gene (>90%) in peripheral blood-derived NK (TIGIT BE-NK) cells. TIGIT editing forced tumor-derived CD155 to engage CD226 and thereby converted an inhibitory signal into an activating one that amplified NK-cell cytotoxicity. TIGIT BE-NK cells specifically targeted cancer cells across multiple tumor types and were validated as safe, with minimal off-target effects. Cryopreserved TIGIT BE-NK cells exhibited similar antitumor activity as fresh TIGIT BE-NK cells, supporting their potential as an "off-the-shelf" therapy. Combining TIGIT BE-NK cells and IL2 further improved antitumor immunity. Together, these results underscore the feasibility of using base editing to modify NK cells and significantly enhance their therapeutic potential for treating patients with cancer. SIGNIFICANCE: Modifying a single base within the TIGIT gene in NK cells switches inhibitory signaling to an activating axis that enhances antitumor immunity, supporting base editing of immune cells as an immunotherapeutic strategy.
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.