• melanoma
• cell death
• cell biology

In 2011, the US Food and Drug Administration (FDA) approved a novel therapy for advanced melanoma: a BRAF inhibitor, called Vemurafenib (or Plx4032), which exclusively affects cells that carry BRAFV600E mutation, the most frequent mutation in melanoma. . The aim of my thesis was to characterise the responses BRAFV600E mutated human melanoma cell lines to Plx4032 (Vemurafenib), with an emphasis on the evaluation of the immunogenic features of the cell death modality induced by this BRAF inhibitor. For this purpose, I analysed and compared two human cell lines: one harbouring the BRAFV600E mutation (A375) and therefore Plx4032-sensitive, and another one carrying the wild-type BRAF (MM031), which could reveal possible off-target effects of the RAF inhibitor.