ArticleNature communications2024
Targeting branched N-glycans and fucosylation sensitizes ovarian tumors to immune checkpoint blockade.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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
23 citing papers in PubMed.
- Immune implications and therapeutic opportunities of tumor glycosylation.Nature cancer · 2026Review
- Parkinson's Disease-Associated Remodeling of SynapticJournal of proteome research · 2026Article
- Review
- L-Fucose: a dietary sugar with multifaceted potential in the biology and therapy of cancer.Nature reviews. Cancer · 2026Review
- Distinct Proteomic and Glycosylation Signatures Differentiate A549 Tumor and BEAS-2B Nontumor Cell Line-Derived Small Extracellular Vesicles.Molecular & cellular proteomics : MCP · 2026Article
- FUT8 Catalysis Involves GDP-Fucose-Induced Loop Activation Promoting a Reaction at the SACS catalysis · 2026Article
- Sweet Surprises: Decoding Tumor-Associated Glycosylation in Cancer Progression and Therapeutic Potential.Cells · 2026Review
- Models of high-grade serous carcinoma of tubo-ovarian origin.Oncology reviews · 2026Review
- Structure, function, and implications of fucosyltransferases in health and disease.Nature communications · 2025Review
- Tumor desialylation surpasses anti-PD-L1 checkpoint therapy in restoring anti-tumor immunity in a murine model for colorectal cancer.International journal of cancer · 2025Article
- Constructing a Prognostic Model for Clear Cell Renal Cell Carcinoma Based on Glycosyltransferase Gene and Verification of Key Gene Identification.International journal of molecular sciences · 2025Article
- Post-translational modifications in ovarian cancer: implications for immunotherapy: a mini-review.Journal of ovarian research · 2025Review
- Analytical dissection of minor glycoforms and glycoprotein associations in rAAV preparations by multimodal glycoproteomics.Analytical and bioanalytical chemistry · 2025Article
- Glycosylation in cancer: mechanisms, diagnostic markers, and therapeutic applications.Molecular and cellular biochemistry · 2025Review
- N-glycans in lung tissue specimens: a prospective target for enhanced cancer diagnosis and prognosis.Journal of translational medicine · 2025Article
- Longitudinal study reveals plasma glycans associations with prediabetes/type 2 diabetes in KORA study.Cardiovascular diabetology · 2025Article
- Article
- sEV-mediated intercellular transformation from MGAT4AOncogene · 2025Article
- Upregulation of Sulfated N-Glycans in Serum as Predictive Biomarkers for Early-Stage Breast Cancer.International journal of molecular sciences · 2025Article
- Regulatory T Cell Metabolism: A Promising Therapeutic Target for Cancer Treatment?Immune network · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
19 authors.
Funding
Abstract
Aberrant glycosylation is a crucial strategy employed by cancer cells to evade cellular immunity. However, it's unclear whether homologous recombination (HR) status-dependent glycosylation can be therapeutically explored. Here, we show that the inhibition of branched N-glycans sensitizes HR-proficient, but not HR-deficient, epithelial ovarian cancers (EOCs) to immune checkpoint blockade (ICB). In contrast to fucosylation whose inhibition sensitizes EOCs to anti-PD-L1 immunotherapy regardless of HR-status, we observe an enrichment of branched N-glycans on HR-proficient compared to HR-deficient EOCs. Mechanistically, BRCA1/2 transcriptionally promotes the expression of MGAT5, the enzyme responsible for catalyzing branched N-glycans. The branched N-glycans on HR-proficient tumors augment their resistance to anti-PD-L1 by enhancing its binding with PD-1 on CD8
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.