We focus on the molecular pathophysiology of pancreatic ductal adenocarcinoma (PDAC) and urothelial bladder carcinoma (UBC) taking a disease-oriented approach. These tumours present very distinct clinical challenges. We learn from patient samples, cultured cells/organoids, and genetically modified mice. To translate the findings, we bring this knowledge to a “population” level leveraging on information and samples from large patient cohorts together with Núria Malats (CNIO).
PDAC has a dismal prognosis even when diagnosed early. We aim to dissect the molecular mechanisms involved in very early steps of tumour development, harnessing the excellent genetic mouse models available. A main hypothesis is that cell differentiation is an early and potent tumour suppressor mechanism. Understanding the contribution of early molecular events is crucial to design better strategies for prevention and early tumour detection.
UBC presents with very wide clinical and pathological heterogeneity. We aim to acquire knowledge about the underlying molecular pathways and to apply it for improved prediction of outcome and therapy.