ReviewCancers2018
Hypersialylation in Cancer: Modulation of Inflammation and Therapeutic Opportunities.
Review in Cancers, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 117 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
117 citing papers in PubMed, 235 citations in OpenAlex.
- Aberrant sialylation in cancer: From molecular mechanisms to potential therapeutics.Genes & diseases · 2026Review
- Galectin-3 Mediates TGF-β-Controlled Migration in Müller Glial Cells.International journal of molecular sciences · 2026Article
- Article
- Rapid discovery of cell-surface glycosylation regulators using a lectin-based magnetic CRISPR screen.Cell reports methods · 2026Article
- The microenvironment dictates glyco-immune surveillance via HSF1-mediated metabolism.Science advances · 2026Article
- Association of B3GNT3 Expression with Tumour Stage and Lymph Node Metastasis in Colon Adenocarcinoma.International journal of molecular sciences · 2026Article
- Nanotechnology-mediated strategies for skeletal muscle repair and regeneration: targeted intervention, functional remodeling, and translational challenges.Journal of nanobiotechnology · 2026Review
- Dietary Fructose Alters Duodenal Mucin Glycosylation and Mucus Production in High-Fat Diet-Fed Mice.International journal of molecular sciences · 2026Article
- Inhibition of endocytosis by glycans arises from steric rather than electrostatic repulsion.Biophysical journal · 2026Article
- CRISPR activation screens map the genomic landscape of cancer glycome remodeling.Cell genomics · 2026Article
- GlycoChat Uncovers Glycan-Lectin Circuits in the Tumor Microenvironment of Pancreatic Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Writers and readers of sialylation in immunoregulation in cancer.The Journal of biological chemistry · 2026Review
- Nanoparticles co-loaded with bacillus Calmette-Guérin pure protein derivative and doxorubicin for bladder tumor therapy.BMC biotechnology · 2026Article
- Multifaceted elucidation of aminoguanidine in protecting against diabetes-induced vascular endothelial injury.Acta biochimica et biophysica Sinica · 2026Article
- Advancements on the synergistic application of oncolytic viruses and molecularly targeted therapies for the treatment of solid tumors (Review).International journal of oncology · 2026Review
- Article
- Simultaneous ManNAc and Neu5Ac Quantification in Human Sera by LC-MS/MS.International journal of molecular sciences · 2026Article
- Targeting Interactions Between Siglec-10 and α3β1 Integrin Enhances Macrophage-Mediated Phagocytosis of Pancreatic Cancer.Cancer research · 2026Article
- Hematologic Glyco-Signatures: Emerging Blood-Based Sugar Codes Linked to Hyper-Aggressive Breast Cancer.Breast cancer (Dove Medical Press) · 2026Review
- Transmembrane lectins in cancer immunity: emerging drivers of myeloid-mediated immunosuppression.Frontiers in immunology · 2026Review
57 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Cell surface glycosylation is dynamic and often changes in response to cellular differentiation under physiological or pathophysiological conditions. Altered glycosylation on cancers cells is gaining attention due its wide-spread occurrence across a variety of cancer types and recent studies that have documented functional roles for aberrant glycosylation in driving cancer progression at various stages. One change in glycosylation that can correlate with cancer stage and disease prognosis is hypersialylation. Increased levels of sialic acid are pervasive in cancer and a growing body of evidence demonstrates how hypersialylation is advantageous to cancer cells, particularly from the perspective of modulating immune cell responses. Sialic acid-binding receptors, such as Siglecs and Selectins, are well-positioned to be exploited by cancer hypersialylation. Evidence is also mounting that Siglecs modulate key immune cell types in the tumor microenvironment, particularly those responsible for maintaining the appropriate inflammatory environment. From these studies have come new and innovative ways to block the effects of hypersialylation by directly reducing sialic acid on cancer cells or blocking interactions between sialic acid and Siglecs or Selectins. Here we review recent works examining how cancer cells become hypersialylated, how hypersialylation benefits cancer cells and tumors, and proposed therapies to abrogate hypersialylation of cancer.
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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.