ReviewExperimental dermatology2026
CD24 in Melanoma: Biomarker, Innate Immune Checkpoint and Emerging Therapeutic Target.
Review in Experimental dermatology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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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
2 citing papers in PubMed.
- Evasion of cell death despite mitochondrial outer membrane permeabilization: an oncogenic outcome of apoptosis.Apoptosis : an international journal on programmed cell death · 2026Review
- Glycosylation converts CD24 from a developmental marker into a glyco-immune checkpoint in B-cell acute lymphoblastic leukemia.Frontiers in immunology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Immune checkpoint inhibitors have transformed the treatment of advanced melanoma, yet many patients develop primary or acquired resistance. Although most work has focused on adaptive checkpoints (PD-1 and CTLA-4), accumulating evidence implicates innate immune suppression and stem-like, drug-resistant melanoma cell states. CD24, a small, heavily glycosylated glycosylphosphatidylinositol (GPI)-anchored surface protein, sits at the intersection of these processes and is emerging as a context-dependent biomarker and potential mediator of aggressive, therapy-resistant melanoma states. In this review, we synthesize evidence indicating that CD24 is both a tumour-intrinsic and tumour-extrinsic regulator in melanoma. We summarize the structure, glycosylation and regulation of CD24, then discuss its role in melanoma, supporting phenotypic plasticity, sustaining stem-like populations and promoting resistance to BRAF-targeted and cytotoxic therapies through SOX2/STAT3-linked programmes. We then examine the CD24-Siglec-10 axis as an innate immune checkpoint that suppresses macrophage and dendritic cell function, promotes immune-excluded 'cold' tumour microenvironments and may shape responses to immunotherapy among CD24+ melanoma cells. We highlight CD24 in tumour tissue, blood and extracellular vesicles as potential biomarkers of prognosis and pathway activity, and review CD24-axis interventions, including anti-CD24 antibodies, Siglec-10 antagonists and CD24-targeted CAR-T/CAR-NK cells, with rational combinations alongside PD-1/CTLA-4 blockade and MAPK-targeted therapy. We propose that biomarker-driven trials targeting this axis could open a new front in melanoma immunotherapy.
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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.