ArticleCell genomics2026
CRISPR activation screens map the genomic landscape of cancer glycome remodeling.
Article in Cell genomics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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
8 citing papers in PubMed.
- Review
- Rapid discovery of cell-surface glycosylation regulators using a lectin-based magnetic CRISPR screen.Cell reports methods · 2026Article
- CRISPR activation screens identify core protein-dependent regulation of heparan sulfate sulfation and ligand specificity.bioRxiv : the preprint server for biology · 2026Article
- Siglec-G on B cells restrains the germinal center response by controlling T cell help during positive selection.bioRxiv : the preprint server for biology · 2026Article
- Revealing cancer glycome drivers using CRISPR activation screens.Cell genomics · 2026Article
- Writers and readers of sialylation in immunoregulation in cancer.The Journal of biological chemistry · 2026Review
- Immunological and pathological roles of Siglecs: a molecular review.Frontiers in immunology · 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
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Many cancers upregulate the expression of sialic acid-containing glycans. These oligosaccharides engage inhibitory sialic acid-binding immunoglobulin-like lectin (Siglec) receptors on immune cells, allowing cancer cells to evade immune surveillance. The genetic mechanisms underlying this process remain poorly defined. In this study, we performed gain-of-function CRISPR activation (CRISPRa) screens to define genetic pathways that regulate expression of Siglec-binding glycans. We show that Siglec ligand expression is controlled through genetic competition between genes that catalyze α2-3 sialylation and GlcNAcylation of galactose residues. Cancer glycome remodeling is also aided by the overexpression of "professional ligands" that facilitate Siglec-glycan binding. Notably, we also find that expression of the CD24 gene is genetically dispensable for cell surface binding of the inhibitory receptor Siglec-10. Finally, we identify the sulfotransferase enzyme GAL3ST4 as a potential driver of immune evasion in glioma cells. Our study provides a unique genomic atlas of cancer-associated glycosylation and identifies immediately actionable targets for cancer immunotherapy.
Indexed as
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.