Prostate cancer is the most commonly diagnosed malignancy among men and the second leading cause of cancer-related mortality in developed countries. While a majority of patients face very favorable outcomes and are unlikely to succumb from the disease, a subset will progress to more aggressive forms that are highly metastatic and lethal. In these cases, treatment options are initially effective but therapeutic resistance eventually occurs leading to an associated mortality.

My laboratory aims at uncovering new mechanisms driving cancer progression and metastasis and to elucidate how these mechanisms contribute to the emergence of therapeutic resistance. The lab´s main focus is on prostate cancer utilizing genetically-engineered mice (GEM) to model relevant molecular alterations, thereby recapitulating the progression pathway observed in human prostate cancer. In addition, our lab utilizes gene regulatory network-based approaches to conduct cross-species studies to identify actionable targets that can be validated in preclinical models.

The research in our lab focuses on understanding how the landscape of genetic and epigentic alterations shape dinamic changes in gene repulatory programs that ultimately result in the selection or emergence of therapeutic resistance to standard of care treatments, mainly androgen deprivation and  androgen receptor targeting approaches. The specific research lines in the lab cover different aspects:

1. We want to elucidate cell cycle independent mechanims by which the FOXM1 and CENPF master regulators contribute to the  acquisition of the lethal metastatic phenotype and therapy failure.
2. We are also investigating how the aberrant expression of chromatin modifiers in metastatic castration resistant prostate cancer affects the AR cistrome and contributes to Enzalutamide resistance.
3. We want to generate a comprehensive landscape of chromatin accessibility in advanced and castration resistant prostate cancer to complement the existing transcriptomics and genomics datasets.