ArticleProceedings of the National Academy of Sciences of the United States of America2014
Immature truncated O-glycophenotype of cancer directly induces oncogenic features.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 209 papers, 1 of them a synthesis that pooled it.
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Who cites it
209 citing papers in PubMed, 1 synthesis or guideline pooled it, 317 citations in OpenAlex.
- Pooled it
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- Distinct glycosyltransferase expression governs organ-specific survival in pancreatic cancer metastasis.Oncogene · 2026Article
- From Glycocode to Precision Oncology: Therapeutic Strategies Targeting Aberrant O-GalNAc Glycosylation in Cancer.Chemical reviews · 2026Review
- Glycosylation orchestrates megakaryocytic fate of hematopoietic stem cells via Wnt-MUC13 signaling.Nature communications · 2026Article
- Post-Translational Modifications in Pancreatic Cancer: Mechanisms to Clinical Applications.Journal of gastroenterology and hepatology · 2026Review
- Cancer-associated alterations in O-GalNAc glycosylation.Glycobiology · 2026Review
- Development of Antibody and Antibody Fragment-Based Radiopharmaceuticals for Cancer Imaging and Therapy.Nuclear medicine and molecular imaging · 2026Review
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- Glycosite mapping and in situ mass spectrometry imaging of MUC2 glycopeptides via on-slide mucinase digestion.Nature communications · 2026Article
- Deletion of Core 1 β3GalT-specific molecular chaperone (Cosmc) in murine intestinal epithelia leads to major alterations in glycocalyx and tumorigenesis.The Journal of biological chemistry · 2026Article
- Hemocyte-secreted papilin bearing mucin-typeiScience · 2026Article
- Glycomic Insights in Gynecological Disease: From Molecular Mechanisms to Precision Diagnostics and Therapeutics.International journal of molecular sciences · 2026Review
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- CD276 immature glycosylation drives colorectal cancer aggressiveness and T cell mediated immune escape.Cell communication and signaling : CCS · 2026Article
- CORT silencing impairs migration and invasion: validation of a glycosylation-based risk model (CORT/LPAR5/CEBPA/MYH10/MAGEA11) in osteosarcoma.European journal of medical research · 2026Article
- Mucin-typebioRxiv : the preprint server for biology · 2025Article
- Tuning CAR-T cells by targeting cancer-associated glycan in pancreatic cancer.Nature communications · 2025Article
- Neuromuscular Defects in aBiomolecules · 2025Article
- Unraveling the glyco-immunity nexus in pancreatic cancer.Molecular cancer · 2025Review
149 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
24 authors at 3 institutions in 3 countries.
Funding
Abstract
Aberrant expression of immature truncated O-glycans is a characteristic feature observed on virtually all epithelial cancer cells, and a very high frequency is observed in early epithelial premalignant lesions that precede the development of adenocarcinomas. Expression of the truncated O-glycan structures Tn and sialyl-Tn is strongly associated with poor prognosis and overall low survival. The genetic and biosynthetic mechanisms leading to accumulation of truncated O-glycans are not fully understood and include mutation or dysregulation of glycosyltransferases involved in elongation of O-glycans, as well as relocation of glycosyltransferases controlling initiation of O-glycosylation from Golgi to endoplasmic reticulum. Truncated O-glycans have been proposed to play functional roles for cancer-cell invasiveness, but our understanding of the biological functions of aberrant glycosylation in cancer is still highly limited. Here, we used exome sequencing of most glycosyltransferases in a large series of primary and metastatic pancreatic cancers to rule out somatic mutations as a cause of expression of truncated O-glycans. Instead, we found hypermethylation of core 1 β3-Gal-T-specific molecular chaperone, a key chaperone for O-glycan elongation, as the most prevalent cause. We next used gene editing to produce isogenic cell systems with and without homogenous truncated O-glycans that enabled, to our knowledge, the first polyomic and side-by-side evaluation of the cancer O-glycophenotype in an organotypic tissue model and in xenografts. The results strongly suggest that truncation of O-glycans directly induces oncogenic features of cell growth and invasion. The study provides support for targeting cancer-specific truncated O-glycans with immunotherapeutic measures.
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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.