12:00 – 12:30 Antonio Serrano

Identification of new biomarkers and development of combination polymer conjugates in metastatic prostate cancer

Prostate cancer represents the second most common cancer and the fifth cause of cancer death in men worldwide. Despite immense efforts made in recent decades to discover new therapeutic approaches, the survival rate of patients remains very poor when cancer progression reaches an advanced state, such as in the metastatic castration-resistant phenotype. Current strategies focus on combination therapies targeting different pathways and achieving therapeutic synergism.
Around 20% of advanced prostate cancer patients harbor DNA repair pathway aberrations, with tumor cells relying on poly (ADP-ribose) polymerase (PARP) to fix any DNA damage. While the administration of PARP inhibitors in prostate cancer patients in advanced stages has met some success, these drugs can induce side effects such as anemia, neutropenia, and thrombocytopenia and patients can develop resistance to these drugs through a range of mechanisms.
The field of nanomedicine has developed promising approaches for disease treatment, diagnosis, and monitoring. Nanomedicines have the potential to significantly improve cancer treatment by decreasing drug toxicity and overcoming drug resistance, among other advantages. Therefore, we aimed to evaluate combination therapies based on PARP inhibitors to treat advanced prostate cancer patients by synthesizing and evaluating novel combinatorial polypeptide-drug conjugates in two-dimensional, advanced three-dimensional, and in vivo models.

12:30 – 13:00 Noelia Pimentel

Dissecting retinal degeneration in Cohen syndrome

Cohen Syndrome (CS) is a rare genetic disorder characterized by heterogeneous, multi-system pathology involving retinal dystrophy. CS is caused by autosomal recessive mutations in the VPS13B (VACUOLAR PROTEIN SORTING 13 HOMOLOG B) gene. VPS13B localizes to the Golgi complex and roles in vesicular trafficking and lipid transfer at membrane contact sites between organelles have been suggested. Furthermore, VPS13B depletion has shown impairments in Golgi structure, glycosylation and lipidic alterations, autophagy defects and affected lysosomes. How these defects may be mechanistically linked to retinal dysfunction is not known. The lack of retinal phenotype in available animal models warrants establishing human tissue mimics. My thesis objective is to establish a human retinal disease model using CS patient derived induced pluripotent stem cells in which to study the molecular and cellular events in order to decipher the pathomechanism of retinal degeneration and hence pave the way toward therapeutic solutions.