ArticleTranslational cancer research2026
Midkine restrains T-cell mediated anti-tumor immunity by suppressing macrophage M1 polarization in lung adenocarcinoma.
Article in Translational cancer research, 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
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Lung adenocarcinoma (LUAD) is characterized by a highly immunosuppressive tumor microenvironment (TME), which limits the efficacy of current anti programmed cell death protein 1 (anti-PD-1) immunotherapy. Midkine (MDK), a heparin-binding growth factor, is frequently overexpressed in various malignancies; however, its specific role in regulating anti-tumor immunity in LUAD remains unclear. This study aimed to investigate the immunomodulatory role of MDK in LUAD, and to evaluate the therapeutic potential of MDK neutralization. Methods: In this study, we analyzed single-cell sequencing datasets and validated MDK expression across multiple non-small cell lung cancer (NSCLC) cell lines. To explore the immunomodulatory functions of MDK, we established Results: We confirmed that MDK is significantly upregulated in malignant LUAD cells compared to normal lung epithelial cells. Functional analysis revealed that MDK signaling suppresses T cell-mediated anti-tumor immunity by inhibiting the expansion of cytotoxic CD8 Conclusions: Our findings demonstrate that MDK acts as a key regulator in the LUAD TME by simultaneously restraining T cell activation and M1 macrophage polarization. These data suggest that targeting MDK offers a promising therapeutic strategy to overcome immune suppression and improve clinical outcomes in LUAD.
Indexed as
Identifiers
What Socratic 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 Socratic graph.