ReviewDiscover oncology2026
Therapeutic targeting of cancer stem cell-specific surface glycans and glycoproteins.
Review in Discover oncology, 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.
- Cancer stem cells and drug resistance in cancer: molecular mechanisms and therapeutic targets.Molecular biomedicine · 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
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cancer stem cells (CSCs) represent a critical subpopulation within tumors, driving malignancy, metastasis, and therapeutic resistance. Their unique biological attributes, particularly the distinctive landscape of surface glycans and glycoproteins, offer promising avenues for targeted therapeutic intervention. This comprehensive review explores the pivotal role of CSC-specific surface glycans and glycoproteins, including CD133, CD44 variants, EpCAM, MUC1, gangliosides (GD2, GD3), and truncated O-glycans (Tn, Sialyl Lewis X), as key drivers of CSC properties and therapeutic vulnerabilities. The report details current therapeutic strategies, such as monoclonal antibodies, antibody-drug conjugates, and advanced chimeric antigen receptor (CAR) T, NK, and NKT cell therapies, which are engineered to exploit these surface markers. Furthermore, it examines small molecule inhibitors that target CSC metabolism (metabostemness, the metabolic reprogramming that supports CSC stemness) and induce ferroptosis, a form of regulated cell death characterized by iron-dependent lipid peroxidation, often synergistically. Significant challenges in clinical translation, including achieving specificity, overcoming tumor heterogeneity, modulating the immunosuppressive tumor microenvironment, and addressing manufacturing complexities, are critically discussed. The integration of multi-modal diagnostics, combining multiple diagnostic approaches, encompassing liquid biopsy, advanced imaging, and single-cell epigenomics, is presented as an essential future direction for precision oncology, enabling real-time monitoring and personalized treatment strategies for high-risk cancers like neuroblastoma. This review underscores the imperative for innovative, multi-pronged approaches to effectively eradicate CSCs and achieve durable patient responses.
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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.