Speaker: Kimberley McGrail, is currently a Postdoctoral Researcher at the Biomedical Research in Melanoma Group (VHIR). She studied Biology at the University of Málaga and then she moved to Barcelona to do a master in Advanced Genetics at the University of Barcelona (UAB). She did her PhD in the group of Biomedical Research in Melanoma and nowadays she is working in the lab as a postdoctoral researcher.

BRAFV600E-induced cell growth arrest in melanocytic nevus is on debate where only one third of melanomas arise directly from nevi. We showed that simultaneous neonatal oncogene (BRAFV600E) activation and UVB irradiation prevent BRAFV600E-induced growth arrest in melanocytes, allowing melanoma development. A meta-analysis of gene expression profiles of melanocytes isolated from different mouse models and numerous studies revealed multiple common genes and processes involved in preventing BRAFV600E-induced growth arrest. In humans, many of these genes are associated with poor survival and are upregulated during melanoma progression and in many RAS pathway activation-driven tumors. Single-cell profiling confirmed that BRAFV600E and the identified genes cooperate in melanocyte transformation, including the acquisition of multidrug resistance features. Depletion of these genes in vitro and in vivo revealed the utility of the encoded proteins as therapeutic targets. These results support the existence of BRAFV600E-mutated melanomas unassociated with nevus progression and identify targets for melanoma treatment.

Host: Dr. Juan Ángel Recio,  Head of group Biomedical Research in Melanoma  (VHIR)