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Demonstrates how abnormal glycosylation drives cancer spread in tumors, suggesting new therapeutic targets.
This study explores the crucial role of abnormal O- and N-glycosylation (modification of sugar molecules attached to proteins) in cancer progression and metastatic spread. It examines the effect of this deregulation at several stages of tumor development: primary tumor, microenvironment, blood circulation, and extravasation. During most of these stages, cancer cells can interact with platelets. Platelets are no longer simply coagulation agents but entities capable of educating cancer cells by modifying their enzymatic and transcriptional landscape. The possible use of a specific glycoprotein as a biomarker and a glycan common to several cancers as a therapeutic target has also been described.
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Langiu et al. (2026) studied this question.
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