ReviewiScience2026
Rewiring immunity: Midkine's emerging role in cancer immune escape and drug resistance.
Review in iScience, 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.
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
No grant is acknowledged in the PubMed record.
Abstract
Immunotherapy has transformed cancer care, yet durable responses remain limited by mechanisms of resistance driven by tumors and their microenvironment. Midkine (MDK), a secreted heparin-binding growth factor, has recently emerged as a regulator of the cancer-immune interface. While MDK has long been recognized for its roles in cell survival, proliferation, and angiogenesis, new evidence highlights its ability to reprogram the tumor microenvironment by recruiting myeloid-derived suppressor cells, impairing T cell activation, and disrupting antigen presentation. MDK further reinforces immune evasion and therapeutic resistance through crosstalk with immune checkpoints, stromal components, and signaling pathways, including STAT3, PI3K/AKT, and the Wnt/β-catenin pathway. Here, we summarize current knowledge of MDK's immunoregulatory functions across various cancer types and propose a conceptual framework that positions MDK as a converging node linking oncogenic signaling with immune escape. We also discuss emerging translational strategies to inhibit MDK to overcome therapy resistance and enhance patient outcomes.
Indexed as
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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.