Oncogenes, Transcription and Cancer
Bruno Amati
Group Leader
| [email protected] | |
| Location |
Building 13
Floor 1st Via Adamello 16, Milano |
The MYC proto-oncogene and its product, the MYC transcription factor, have a central role in cellular growth control and oncogenesis. In normal cells, MYC is induced by growth-promoting signals, and in turn regulates genes involved in key cellular responses (growth, proliferation, apoptosis, energy metabolism, biosynthetic pathways, etc…). During tumor development, a variety of oncogenic mutations (affecting either the MYC locus, or upstream signaling pathways) can elicit deregulated MYC expression and, as a consequence, the aberrant implementation of MYC-dependent gene expression programs. MYC-driven tumors show “oncogene addiction”, indicating that MYC itself – and presumably a subset of its target genes – are required for tumor maintenance.
Key questions in the field regard the mechanisms through which MYC regulates transcription, the identity of MYC-regulated genes, their function in growth control and tumorigenesis, as well as their potential as therapeutic targets.
Our research addresses these questions based on a combination of advanced biological models, high-throughput “omic” approaches and computational tools. In parallel with our basic research program, we pursue translational studies aimed at the development and pre-clinical validation of innovative therapeutic strategies.
Most Relevant Publications
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Oxidative stress enhances the therapeutic action of a respiratory inhibitor in MYC-driven lymphoma.
EMBO Mol Med, 2023
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Targeting mitochondrial respiration and the BCL2 family in high-grade MYC-associated B-cell lymphoma.
Mol Oncol, 2022
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Integrated requirement of non-specific and sequence-specific DNA binding in Myc-driven transcription.
EMBO J, 2021
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Therapeutic synergy between tigecycline and venetoclax in a preclinical model of MYC/BCL2 double-hit B cell lymphoma.
Sci Transl Med, 2018