ArticleOncogenesis2026
SHP1 expression in tumor-associated dendritic cells drives immunoevasion via impairing CD8
Article in Oncogenesis, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors.
Funding
Abstract
Despite the achievements of immunotherapy in the treatment of cancer, overcoming the immune resistance is still an unmet challenge. Dendritic cells (DCs) dysfunction plays a pivotal role in tumor immunoevasion. Previous study uncovered that targeting src homologous region 2 protein tyrosine phosphatase (SHP1) improved anti-PD-1 therapy efficacy in breast cancer by reinvigorating DCs, but the detailed mechanisms remained unclear. Here, we investigated the function of SHP1 in enabling tumor immune escape and suppressing memory T cell formation. Deficiency of SHP1 augmented the activation and antigen-presenting function of dendritic cells, which consequently suppressed the growth of B16-F10 and EMT6 models. We validated this enhanced DC-mediated anti-tumor immunity using conditional knockout mice of SHP1. These results suggested that SHP1 acts as a critical promoter of tumor immune escape. Combining transcriptomic analysis with DC-specific SHP1 deletion, we demonstrated that SHP1 deficiency augments DC immunogenicity via the IFN-γ-JAK1/2-STAT1 pathway. Furthermore, SHP1 blockade promoted the generation of central memory CD8
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.