SynthesisNaunyn-Schmiedeberg's archives of pharmacology2025
Molecular mechanisms and pathophysiological implications of mucin-type O-glycosylation dysregulation in colorectal cancer progression.
Synthesis in Naunyn-Schmiedeberg's archives of pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed.
- LRMDA promotes intestinal mucosal barrier integrity and limits colitis and colon cancer.iScience · 2026Article
- Mass Spectrometry-Based Proteomics Methods for Systematic Identification and Quantification of Protein O-Glycosylation in Complex Biological Samples.Journal of the American Society for Mass Spectrometry · 2026Review
- Adhesion to aggression: unravelling sLeClinical & experimental metastasis · 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
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Colorectal cancer (CRC) is among the most prevalent malignancies globally, with 1.9 million new cases annually. While CRC pathogenesis has been widely attributed to the adenoma-carcinoma and serrated sequences, our study highlights the critical and multifaceted role of O-glycosylation impairment in this malignancy. Mucin-type O-glycosylation, a key post-translational modification, exerts significant effects on tumor cells, impacting their proliferation, migration, and invasiveness. Additionally, its influence on the immune response to CRC presents novel perspectives for potential therapeutic interventions. The authors conducted a systematic literature review following Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines, using databases such as Google Scholar, PubMed, and Scopus. In this article, we provide a comprehensive analysis of the mechanisms underlying mucin-type O-glycosylation disruption in CRC and examine how these mechanisms could serve as biomarkers for early diagnosis and personalized treatment strategies. Our findings contribute to a more detailed understanding of CRC pathogenesis and offer promising directions for innovative diagnostic and therapeutic approaches, which in the future may lead to improved patient prognosis.
Indexed as
Identifiers
40257491What 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.