Events

The transcription factor MYC, encoded by the c-MYC proto-oncogene, is induced by mitogenic stimuli and drives the activation of biosynthetic and metabolic pathways required for cell growth and proliferation (1). The same pathways are deregulated in MYC-driven tumors and contribute to the malignant phenotype, but concomitantly elicit multiple stresses to which cancer cells must adapt during disease progression. Hence, MYC-overexpressing cells depend on a fragile equilibrium between conflicting signals, which creates opportunities to exploit synthetic lethality as a strategy for targeted therapeutic intervention (2). Over the years, my group has been committed to unravel MYC-regulated gene-expression programs in normal and tumor cells, identify key MYC effectors in tumorigenesis, and exploit this knowledge toward the development of targeted therapies. This seminar will provide an overview of our efforts, summarize the main concepts and illustrate recent breakthroughs in this area. 1. T. R. Kress, A. Sabò, B. Amati, MYC: connecting selective transcriptional control to global RNA production. Nat Rev Cancer 15, 593-607 (2015). 2. G. Donati, B. Amati, MYC and therapy resistance in cancer: risks and opportunities. Mol Oncol 16, 3828-3854 (2022).