ArticleMolecular therapy oncolytics2023
Disruption of CISH promotes the antitumor activity of human T cells and decreases PD-1 expression levels.
Article in Molecular therapy oncolytics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.
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
30 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.
- Strategies and mechanisms for the enhancement of chimeric antigen receptor T-cell functions.Science China. Life sciences · 2026Pooled it
- Non-viral targeted integration at the CISH locus enables CAR-NK cell engineering with enhanced anti-tumor activity.Molecular therapy. Oncology · 2026Article
- Cellular immunotherapy in melanoma: the next frontier in cancer treatment.Journal of experimental & clinical cancer research : CR · 2026Review
- Efficient multiplex non-viral engineering and expansion of polyclonal γδ CAR-T cells for immunotherapy.Molecular therapy : the journal of the American Society of Gene Therapy · 2026Article
- Preventing trogocytosis by cathepsin B inhibition augments CAR T-cell function.Signal transduction and targeted therapy · 2026Article
- Article
- A bibliometric analysis of resistance to PD-1/PD-L1 inhibitors.Frontiers in immunology · 2026Article
- Cytokine inducible SH2-containing protein: a versatile negative regulator of cytokine receptor signaling.Frontiers in immunology · 2026Review
- Harnessing the potential of gene editing technology for CAR-T cell therapy of solid tumors.Inflammation and regeneration · 2025Review
- Liver-Microbiome Crosstalk Mediates the Protective Effects of Artemisinin in Clostridium perfringens Models.Microbial biotechnology · 2025Article
- Base-editing a single missense mutation in A20 enhances CAR-T cell efficacy.bioRxiv : the preprint server for biology · 2025Article
- Special Issue "The Promising Future of CAR-Based Therapies: A Matter of Molecular Details".International journal of molecular sciences · 2025Article
- Preventing trogocytosis by cathepsin B inhibition augments CAR T cell function.bioRxiv : the preprint server for biology · 2025Article
- Recent advances and challenges of cellular immunotherapies in lung cancer treatment.Experimental hematology & oncology · 2025Review
- Article
- Efficient multiplex non-viral engineering and expansion of polyclonal γδ CAR-T cells for immunotherapy.bioRxiv : the preprint server for biology · 2024Article
- Cytoplasmic FBXO38 mediates PD-1 degradation.EMBO reports · 2024Article
- Intracellular checkpoints for NK cell cancer immunotherapy.Frontiers of medicine · 2024Review
- Xianling Lianxia formula improves the efficacy of trastuzumab by enhancing NK cell-mediated ADCC in HER2-positive BC.Journal of pharmaceutical analysis · 2024Article
- Ubiquitin modification in the regulation of tumor immunotherapy resistance mechanisms and potential therapeutic targets.Experimental hematology & oncology · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
16 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tumor cells and the immunosuppressive tumor microenvironment suppress the antitumor activity of T cells through immune checkpoints, including the PD-L1/PD-1 axis. Cytokine-inducible SH2-containing protein (CISH), a member of the suppressor of cytokine signaling (SOCS) family, inhibits JAK-STAT and T cell receptor (TCR) signaling in T and natural killer (NK) cells. However, its role in the regulation of immune checkpoints in T cells remains unclear. In this study, we ablated CISH in T cells with CRISPR-Cas9 and found that the sensitivity of T cells to TCR and cytokine stimulation was increased. In addition, chimeric antigen receptor T cells with CISH deficiency exhibited longer survival and higher cytokine secretion and antitumor activity. Notably, PD-1 expression was decreased in activated CISH-deficient T cells
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.