Epithelial Carcinogenesis Group

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Staff Scientists

  • Miriam Marqués

Post-Doctoral Fellows

  • Elena del Pilar Andrada
  • Irene Felipe
  • Eleonora Lapi
  • Jaime Martínez de Villarreal
  • Cristina Segovia
  • Sladjana Zagorac

Graduate Students

  • Catalina Berca
  • Cristina Bodas
  • Sonia Corral
  • Auba Gayá
  • María Ramal


  • Natalia Del Pozo
  • Leticia Rodríguez

We focus on the molecular pathophysiology of pancreatic ductal adenocarcinoma (PDAC) and urothelial bladder carcinoma (UBC) with a disease-oriented approach. We use patient samples, cultured cells, and genetically modified mice, giving a similar weight to the 3 model systems. Observations made at either of these levels are then extended through additional work. To translate the findings, we bring this knowledge to a ‘population’ level – leveraging on information and samples from large patient cohorts – in close collaboration with Núria Malats’ Group (CNIO).

In PDAC, a main hypothesis is that cell differentiation is a potent tumour suppressor mechanism acting early in carcinogenesis. We use the excellent genetic mouse models available because these processes cannot be readily studied in humans. In mice, PDAC can originate in pancreatic progenitors and in adult acinar and ductal cells. Understanding the contribution of early molecular events is crucial to design better strategies for prevention and early tumour detection.

In UBC, we focus on identifying new genes, using them for improved tumour taxonomy, characterising the mechanisms of action, and applying this knowledge for improved prediction of outcome and therapy.