Sandra van Vliet

Cellular glycosylation is a highly dynamic process that alters upon activation, inflammation, and oncogenic transformation. Considering that 98% of all cell surface molecules are glycosylated, these glycans encompass an enormous amount of information. Within the immune system, the glycan blue prints are decoded by specific glycan-receptors, such as the C-type lectin receptors or the Siglecs. Lectins act as signaling receptors and are thus able to shape immune responses. We study how the interaction between lectin receptors and their cancer-associated glycan ligands, such as Tn antigen and the elevated levels of Sialic acids and Lewis antigens, orchestrates immune evasion during cancer progression.

Key publications

Blanas A et al. FUT9-Driven Programming of Colon Cancer Cells towards a Stem Cell-Like State. Cancers (Basel). 2020;12(9):2580

Cornelissen LAM et al. Tn Antigen Expression Contributes to an Immune Suppressive Microenvironment and Drives Tumor Growth in Colorectal Cancer. Front Oncol. 2020;10:1622

Cornelissen LAM et al. Disruption of sialic acid metabolism drives tumor growth by augmenting CD8(+) T cell apoptosis. Int J Cancer. 2019 144(9); 2290-2302

Blanas A et al. Fucosylated Antigens in Cancer: An Alliance toward Tumor Progression, Metastasis, and Resistance to Chemotherapy. Front Oncol. 2018;8:39

Lenos K et al. MGL ligand expression is correlated to BRAF mutation and associated with poor survival of stage III colon cancer patients. Oncotarget. 2015;6(28):26278-90.

Van Vliet SJ et al. Regulation of effector T cells by antigen-presenting cells via interaction of the C-type lectin MGL with CD45. Nat Immunol. 2006;7(11):1200-8.

Contact details: Email; Phone 020-4448142