Although anti-angiogenic therapies have been pivotal in cancer treatment, a wide variety of tumors fail to respond to these strategies or develop resistance over time. In this context, we identified the galectin-1 (Gal-1)-glycan axis as a compensatory mechanism that preserves tumor vascularization in response to anti-VEGF therapies. This discovery positions Gal-1 as a novel therapeutic target not only in cancer, but also across a broad range of diseases characterized by aberrant vascular phenotypes.
We demonstrated that a Gal-1-neutralizing antibody is able to normalize tumor vasculature while simultaneously enhancing antitumor immunity. More recently, we observed that Gal-1 synchronizes the activation of immune and vascular circuits in myeloid cells and links processes of fibrosis and immunomodulation. Together, these studies open a new horizon in which Gal-1 blockade may represent a strategy to stimulate immune responses and normalize vascular and fibrotic programs across multiple cancer types.
