IFOM Marco Foiani

Marco Foiani

Marco Foiani is Professor of Molecular Biology at the University of Milan and, since 2009, Scientific Director of IFOM, an international cancer center that hosts 20 groups and 300 scientists. Two research groups are operating in IFOM outstations located in Singapore (at ASTAR-p53 Laboratory and at the Mechano Biology Institute of NUS) and one in Bangalore, India, (at inSTEM & NCBS). At IFOM, Foiani is responsible for the research strategic planning, the development of programs aimed at the results reduction into practice and for the establishment of national and international co-operation programs and joint ventures. He is the founder of the European Nanomedicine Foundation (CEN) that aims at supporting multidisciplinary projects/teams in biomedicine. Since 2012 he directs a cancer genetics diagnostic laboratory within Cogentech.

Research interests

Scientific leadership profile

Foiani has studied different cellular processes (translational, chromosome replication, DNA recombination, DNA repair, DNA topology, transcription, autophagy and nuclear envelope dynamics) and regulatory pathways (translational control, cell cycle, checkpoint, sumo and ubiquitin pathways, protein acetylation, gene gating) using a variety of approaches (biochemical, genetic, imaging, genomic, molecular biology). His major contributions are within the fields of chromosome dynamics and genome integrity. His work has contributed to elucidate the ATR and ATM-dependent checkpoint processes controlling the interfaces between DNA replication, recombination, transcription and DNA topology and preventing abnormal chromosome transitions.

Key findings:

  1. ATR/Mec1-mediated controls the stability of stalled replication forks preventing fork reversal (Lopes et al. Nature 2001; Sogo et al. Science, 2002 (with cover and preview));
  2. The identification and characterization of sister chromatid junctions (hemicatenanes) mediating physiological and pathological chromosomal transitions (Lopes et al. Mol Cell 2003; Cotta-Ramusino et al. Mol Cell 2005; Liberi et al. Genes & Dev 2005);
  3. The Cdk1-mediated control of homologous recombination and checkpoint activation (Ira et al. Nature 2004);
  4. The specialized sumoylation pathways controlling hemicatenane metabolism when cells experience DNA damage in S phase (Branzei et al. Cell 2006 (with preview); Branzei et al. Nature 2008);
  5. The identification of genomic clusters undergoing topological transitions to coordinate the clash between replication forks and transcription units (Bermejo et al. Genes & Dev 2007; Bermejo et al. Cell 2009);
  6. ATM/Tel1 controls replication forks encountering DNA breaks or short telomeres (Doksani et al. Cell 2009 (with cover and preview));
  7. The identification of those fragile genomic loci where replication forks converge (Fachinetti et al. Mol Cell 2010 (with cover and preview));
  8. The observation that specialized protein acetylation/deacetylation events couple the DNA damage response to autophagy (Robert et al. Nature 2011 (highlighted in Cell and Science);
  9. ATR/Mec1 controls the stability of replication forks encountering transcribed genes by controlling the association of the transcribed loci to the nuclear pore (Bermejo et al. Cell , 2011 (with preview))
  10. A novel role for ATR in mediating a response to mechanical stress at the nuclear envelope (Kumar et al. Cell , 2014 (highlighted in Nature Reviews in Molecular and Cell Biology)). In collaboration with dr. J.Haber (Brandeis University, USA) he has also contributed to elucidate of mechanisms influencing DNA double strand break (DSB) repair (Ira et al. Cell 2003) and promoting activation and deactivation of the ATR/Mec1 checkpoint in response to DSB formation (Pellicioli et al. Mol Cell 2001; Vaze et al. Mol Cell 2002).

In 2004 he was elected EMBO member and in 2010 member of the Academia Europaea. He is currently a member of the editorial board of Cell.

Scientific Vision

Marco Foiani is Full Professor of Molecular Biology at the Department of Biosciences, University of Milan.