T-cell branched glycosylation as a mediator of colitis-associated colorectal cancer progression: a potential new risk biomarker in inflammatory bowel disease - Takeaways - MDSpire

T-cell branched glycosylation as a mediator of colitis-associated colorectal cancer progression: a potential new risk biomarker in inflammatory bowel disease

  • By

  • Eduarda Leite-Gomes

  • Mariana C Silva

  • Ana M Dias

  • Ângela Fernandes

  • Guilherme Faria

  • Rafaela Nogueira

  • Beatriz Santos-Pereira

  • Henrique Fernandes-Mendes

  • Catarina M Azevedo

  • Joana Raposo

  • Julian López Portero

  • Tania de Alda Catalá

  • Carlos Taxonera

  • Paula Lago

  • Maria J Fernandez-Aceñero

  • Isadora Rosa

  • Ricardo Marcos-Pinto

  • Salomé S Pinho

  • March 15, 2025

  • 0 min

Share

  • 1

    Colitis-associated colorectal cancer (CAC) is a significant risk for patients with inflammatory bowel disease (IBD), with increased cancer risk correlating to disease duration.

  • 2

    Branched N-glycosylation levels in colonic T cells are dynamically regulated and associated with the risk of CAC development in IBD patients.

  • 3

    The study identified a glycosylation switch in T cells that inhibits effective antitumor immune responses during CAC progression.

  • 4

    Deletion of branched N-glycans in Mgat5 knockout mice led to reduced CAC development and enhanced infiltration of CD8+ and γδ T cells.

  • 5

    Branched N-glycosylation levels in inflamed lesions can predict CAC progression, offering a potential biomarker for early identification of high-risk IBD patients.

Original Source(s)

Related Content