CONICET | Buscador de Institutos y Recursos Humanos

Inflammatory Bowel Diseases (IBD), which includes Crohn?s disease and Ulcerative Colitis, are a group of chronic, relapsing and remitting intestinal inflammatory pathologies. Although traditional therapies such as general immunosuppressive agents o ant-TNFα monoclonal antibodies are established as conventional treatments, they present serious drawbacks, such as high costs, lack of specificity or eventual loss of response. IBD has been also subject of interest for its association with an increased risk of colorectal cancer (CRC) development, although the underlying molecular mechanisms are not yet completely understood. Colorectal cancer is a high incident and lethal neoplastic disease, from which 1.5 million people are diagnosed every year and accounts for more than 700,000 yearly deaths worldwide. Although the detailed causes of CRC development and progression are still unclear, CRC is a multifactorial pathology where genetic mutations, diet, inflammation, gut microbiota and intestinal inflammation are crucial factors that modulate the disease outcome. During the last decades, aberrant cell surface glycosylation has been considered an important hallmark of inflammation and tumor progression. Glycosylation changes trigger different biological processes via interaction with glycan-binding proteins such as galectins. We aimed to study the effect of the inflammatory microenvironment over the galectin-glycan interactions and colitis-associated CRC progression.