ReviewJournal for immunotherapy of cancer2025
Second signals for cancer immunotherapy.
Review in Journal for immunotherapy of cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed.
- Enhancing persistence while managing cytokine release syndrome to embrace next-generation CAR-T cell therapy.Journal of translational medicine · 2026Review
- Endogenous CD28 Drives the Persistent Activity of CAR T Cells in Myeloma and Lymphoma Models.Blood cancer discovery · 2026Article
- sMICA/sMICB and Immune Checkpoint in Endometriosis: Toward a Minimally Invasive Diagnostic Model Based on Machine Learning.Biomedicines · 2026Article
- T cell exhaustion in parasitic infections.Frontiers in immunology · 2026Review
- SHP2 in TAMs promoted the survival of gastric adenocarcinoma via suppressing the P38/ERK1/2/SP1/BRD4/STING induced inflammation and ROS.Frontiers in medicine · 2026Article
- CEA-4-1BBL: CEACAM5-Targeted 4-1BB Ligand Fusion Proteins for Cis Co-Stimulation with CEA-TCB.Antibodies (Basel, Switzerland) · 2025Article
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
Abstract
Recent years have seen renewed appreciation of the critical role played by the prototypic T cell co-stimulatory receptor CD28 in cancer immunotherapy. Inhibition of co-stimulation by direct competition, as exemplified by cytotoxic T-lymphocyte associated protein 4 (CTLA-4) competition with CD28 for B7 ligands, or interference with intracellular signaling, such as that mediated by SHP2 phosphatase recruited to programmed cell death protein-1 (PD-1), provides tumors with a means to avoid elimination by cytotoxic T cells. Reversing this inhibition or providing co-stimulation by alternative means-bispecific antibodies, chimeric antigen receptors, etc-is the mechanistic basis behind the success of many modern cancer immunotherapies. As such, understanding the complexities of T cell co-stimulation and the various receptors driving it has taken on new importance. In this commentary, we highlight recent studies in this space and discuss their contributions to our understanding of T cell co-stimulatory receptors in cancer.
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.