Saverio Minucci
e-mail: saverio.minucci AT ieo.eu
affiliation: IFOM-IEO Campus-Universita' di Milano
research area(s): Cancer Biology, Genetics And Genomics
Course:
Molecular Medicine: Molecular Oncology and Computational Biology
University/Istitution: Università di Milano, UNIMI-SEMM
University/Istitution: Università di Milano, UNIMI-SEMM
1982-1988 University of Naples MD (with honors) Medical Studies
1988-1991 University of Naples Specialty Oncology
1988-1991: AIRC Fellow, Institute of Pathology, 1st School of Medicine, University of Naples. Discipline: biochemistry, transformation of estrogen receptors.
1992-1994: Visiting Fellow, LMGR, NICHD, National Institutes of Health, Bethesda, USA. Discipline: molecular and cell biology, retinoid receptors.
1994-1997: Visiting Associate, LMGR, NICHD, National Institutes of Health, Bethesda, USA. Discipline: molecular and cell biology, retinoid receptors.
1998-2002: FIRC Scholar, Assistant, Dept of Experimental Oncology, European Institute of Oncology, Milan. Discipline: molecular oncology, mechanisms of leukemogenesis.
2002-present: Associate Professor of Pathology, University of Milan.
2003-present: Group Leader, Dept of Experimental Oncology, Milan.
1988-1991 University of Naples Specialty Oncology
1988-1991: AIRC Fellow, Institute of Pathology, 1st School of Medicine, University of Naples. Discipline: biochemistry, transformation of estrogen receptors.
1992-1994: Visiting Fellow, LMGR, NICHD, National Institutes of Health, Bethesda, USA. Discipline: molecular and cell biology, retinoid receptors.
1994-1997: Visiting Associate, LMGR, NICHD, National Institutes of Health, Bethesda, USA. Discipline: molecular and cell biology, retinoid receptors.
1998-2002: FIRC Scholar, Assistant, Dept of Experimental Oncology, European Institute of Oncology, Milan. Discipline: molecular oncology, mechanisms of leukemogenesis.
2002-present: Associate Professor of Pathology, University of Milan.
2003-present: Group Leader, Dept of Experimental Oncology, Milan.
I have focused our activities on the study of deregulation of chromatin structure/function in cancer for two main reasons:
It is becoming increasingly clear that the deregulation of chromatin modifiers plays a critical role in tumorigenesis;
The use of "potential drugs" which interfere with chromatin modifying enzymes (histone deacetylases, DNA methyltransferases) may be beneficial for clinical treatment of cancer patients (several molecules are progressing through clinical trials).
Thus, I see here an extremely appealing opportunity to perform a mechanistically oriented analysis ("to understand how things happen") that can immediately be applied to better treat the patients ("to try to change things, when they have gone bad"). In fact, a primary focus of my work is to start and implement a contact with the clinical Departments in the European Institute of Oncology, and with biotech companies/pharma companies developing mechanism-based drugs, to have a constant "bi-directional flow" of interactions. The ultimate goal: to go towards a group that considers Man as the primary model system.
It is becoming increasingly clear that the deregulation of chromatin modifiers plays a critical role in tumorigenesis;
The use of "potential drugs" which interfere with chromatin modifying enzymes (histone deacetylases, DNA methyltransferases) may be beneficial for clinical treatment of cancer patients (several molecules are progressing through clinical trials).
Thus, I see here an extremely appealing opportunity to perform a mechanistically oriented analysis ("to understand how things happen") that can immediately be applied to better treat the patients ("to try to change things, when they have gone bad"). In fact, a primary focus of my work is to start and implement a contact with the clinical Departments in the European Institute of Oncology, and with biotech companies/pharma companies developing mechanism-based drugs, to have a constant "bi-directional flow" of interactions. The ultimate goal: to go towards a group that considers Man as the primary model system.
- Interplay between oncogene-induced DNA damage response and heterochromatin in senescence and cancer. Di Micco R, et al. Nature Cell Biology VOLUME 13 | NUMBER 3 | MARCH 2011
- HDACs link the DNA damage response, processing of double-strand breaks and autophagy. Robert T. et al, Nature. 2011 Mar 3;471(7336):74-9.
- The self-association coiled-coil domain of PML is sufficient for the oncogenic conversion of the retinoic acid receptor (RAR) alpha. Occhionorelli M, et al. Leukemia. 2011 May;25(5):814-20
- Pathology tissue-chromatin immunoprecipitation, coupled with high throughput sequencing allows the epigenetic profiling of patient samples. Fanelli M, et al. PNAS USA 2010 Nov 24
- The tumor suppressor p53 regulates polarity of self renewing divisions in mammary stem cells. Cicalese A, et al. Cell 2009 Sep 18; 138(6): 1083-95.
- Cell-cycle restriction limits DNA damage and maintains self-renewal of leukaemia stem cells. Viale A, et al. Nature. 2009 Jan 1;457:51-6
- NA-Seq: a discovery tool for the analysis of chromatin structure and dynamics during differentiation. Gargiulo G, et al. Dev Cell. 2009 Mar;16:466-81
- HDACs link the DNA damage response, processing of double-strand breaks and autophagy. Robert T. et al, Nature. 2011 Mar 3;471(7336):74-9.
- The self-association coiled-coil domain of PML is sufficient for the oncogenic conversion of the retinoic acid receptor (RAR) alpha. Occhionorelli M, et al. Leukemia. 2011 May;25(5):814-20
- Pathology tissue-chromatin immunoprecipitation, coupled with high throughput sequencing allows the epigenetic profiling of patient samples. Fanelli M, et al. PNAS USA 2010 Nov 24
- The tumor suppressor p53 regulates polarity of self renewing divisions in mammary stem cells. Cicalese A, et al. Cell 2009 Sep 18; 138(6): 1083-95.
- Cell-cycle restriction limits DNA damage and maintains self-renewal of leukaemia stem cells. Viale A, et al. Nature. 2009 Jan 1;457:51-6
- NA-Seq: a discovery tool for the analysis of chromatin structure and dynamics during differentiation. Gargiulo G, et al. Dev Cell. 2009 Mar;16:466-81
Project Title:
Molecular pathogenesis and epigenetic therapy of cancer
Recently we have given seminal contributions to the comprehension of the molecular pathogenesis of acute promyelocitic leukemia, showing that aberrant recruitment of histone deacetylases and other chromatin modifiers by oligomeric leukemia fusion proteins is a key leukemogenic event. At the present we have started the characterization of cancer initiating and stem cells in APL, providing new models for the study of the epigenome of these subpopulations. The characterization of cancer initiating and stem cells in APL will be pivotal in the studies performed with epigenetic drugs (which may target or not these cell populations).