#IDIBELLfellows: Javier Sigüenza & Marta Hernández

ATM-defective murine prostate cancer models recapitulates the PARP inhibition response in patients
Javier Sigüenza Andrade
Resistance and progression mechanisms in prostate cancer group
Prostate cancer remains the most frequently diagnosed cancer and the second leading cause of cancer-related death in men. Approximately 30% of patients progress to an aggressive stage known as metastatic castration-resistant prostate cancer (mCRPC), for which no curative treatments exist. Genomic studies have revealed that nearly 30% of mCRPC tumors harbor defects in the DNA damage response pathway, with BRCA2 and ATM being the most commonly altered genes. Both genes are part of the homologous recombination repair (HRR) pathway, whose inactivation is predicted to sensitize tumors to PARP inhibition. However, clinical trials testing PARP inhibitors in mCRPC patients have shown strong responses in BRCA2-deficient tumors but limited benefit in those with ATM loss. Here, we have modeled ATM loss using genetically engineered mouse models of prostate cancer to investigate the molecular mechanisms underlying resistance to PARP inhibition in this context.

POST-COVID interstitial changes and the role of antifibrotic treatment
Marta Hernandez Argudo
Pneumology group
The aim is to understand the predisposing factors for patients who suffered severe pneumonia due to Covid-19 (admission to a semi-critical and/or critical care unit) to present interstitial pulmonary sequelae of the “fibrosis-like” type, as well as the evolution over time that these patients have had both at the radiological level and in lung function and whether antifibrotics (currently approved for Idiopathic Pulmonary Fibrosis and Progressive Pulmonary Fibrosis) can provide any benefit for the recovery of these patients.