“…These studies demonstrate that there is a downregulation in the tumour tissue of glypican-3 and syndecan-1 [25], an underrepresentation of complex N-glycans and α2,3-sialylation [126], a decrease of bisecting GlNAcylation, Lewis-type fucosylation [127], 9 N-glycans (M/Z 973 2+ , 1055 2+ , 1060 2+ , 1075 2+ , 1162 2+ , 1177 2+ , 1264 2+ , 1279 2+ , 1352 2+ ) [128], and a decrease of fucosylation levels and highly branched N-glycans in stage II CRC [129]. On the other hand, there is an increase in tumour tissue of glucosylceramide, lactosylceramide, monosialic acid ganglioside, globoside 4 [25], chondroitin sulphate, dermatan sulphate [130], high mannose, hybrid and paucimannosidic type N-glycans [126], α2,6-sialylation together with an increase in total sialylation in mid-to late tumours, mannose type N-glycan structures [127], glycan-Tn/STn-MUC1 [131], 3 N-glycans (M/Z 1013 2+ , 1116 2+ , 1228 2+ ) [128], overrepresentation of oligomannosidic, bi-antennary hypogalactosylated and branched compositions [100], and an increase in stage II CRC of sialylation levels and high-mannose glycans [129]. All biomarkers are summarized in Table 6.…”