Pancreatic ductal adenocarcinoma (PDAC)

PDAC is the most common subtype of pancreatic cancer and the solid tumor with the poorest prognosis, with a 5-year survival rate below 10%. It is currently the third leading cause of cancer-related death in developed countries and is projected to become the second by 2030. Although immunotherapy has transformed the treatment of several cancers, its efficacy in PDAC remains very limited due to a highly immunosuppressive and desmoplastic tumor microenvironment that drives therapeutic resistance.

Understanding the molecular mechanisms governing tumor microenvironment dynamics is essential for developing new treatment strategies for this devastating disease. We have demonstrated that galectin-1 (Gal-1) hierarchically regulates multiple events involved in PDAC biology, including tumor cell proliferation, invasion, angiogenesis, inflammation, and metastasis.

Using patient-derived spheroids and organoids, we design and evaluate strategies targeting the Gal-1–glycan axis. Our goal is to reprogram the tumor microenvironment, enhance T-cell responses, and sensitize tumors to combination therapies. This approach aims to advance toward more precise and effective immunotherapy in PDAC, with the potential to achieve meaningful improvements in patient survival.