Scientific topics
Keywords
ITMO
JEROME TORRISANI PhD. Molecular biology and Epigenetics
Course and current status
Jérôme TORRISANI, PhD
Senior Scientist INSERM
CURRENT POSITION
Senior Scientist (CRCN-INSERM) (Since Oct. 2010)
Team: ImPact- Therapeutic innovation in pancreatic cancer
Cancer Research Center of Toulouse (France)-Inserm U1037
BIOGRAPHICAL
Date of birth: August 4th, 1974
City of birth : Romagnat, France
Marital status: Married, one child
Citizenship: French
MAILING ADRESS
Cancer Center of TOULOUSE/Centre de Recherches en Cancérologie de Toulouse
UMR1037 INSERM-Université Toulouse 3-ERL 5294 CNRS
1, avenue Jean Poulhès
31432 TOULOUSE cedex 4
Phone : +33 5 61 32 24 09
Fax : + 33 5 61 32 24 03
EDUCATION
2007-2010 Post-doctoral position.
Institute of Health and Medical Research (INSERM) Unit 858.
Molecular Medicine Institute of Rangueil.
Supervisor: Pr. Louis Buscail, MD, PhD.
2002-2007 Post-doctoral position.
McGill University-Montreal, Canada.
Department of pharmacology and therapeutics.
Supervisor: Dr. Moshe Szyf, PhD.
2002 Ph. D in Human Physiopathology.
Paul Sabatier University-Toulouse, France.
Institute of Health and Medical Research (INSERM) Unit 531.
Title : Molecular mechanisms involved in the loss of SST2 somatostatin receptor gene expression in human pancreatic cancer cells. Supervisor: Dr Louis Buscail MD, PhD.
1998 Master in Human Physiopathology.
Paul Sabatier University-Toulouse, France.
1997 Military service done from October 1996 to July 1997.
92nd infantry regiment-Clermont-Ferrand, France.
1996 Four-year university degree.
Blaise Pascal University-Clermont-Ferrand, France.
Scientific summary
Pancreatic cancer, or pancreatic adenocarcinoma (PDAC), will soon become the second leading cause of cancer deaths worldwide, due to late diagnosis and lack of effective treatment. Our research effort is dedicated to the development of new strategies to improve the management of patients with this cancer. In this context, our research objective is to better understand the mechanisms of PDAC oncogenesis and therapeutic resistance. In particular, we are studying the role of genome remodelling and replication in gene expression and resistance to DNA-breaking agents.
The level of genome compaction is controlled by numerous epigenetic modifications and chromatin remodelling proteins. Many of these are altered in pancreatic cancer cells (e.g. ARID1A/B, SMARCA4, etc.). This level of compaction largely conditions gene expression. Our research focuses on chromatin remodelling and epigenetic modifications, which impact genome organisation and gene expression during pancreatic carcinogenesis. Moreover, chromatin decondensation is an essential mechanism for the repair of DNA breaks induced by most chemo- and radio-therapies. Thus, we are studying the influence of the level of genome compaction on the sensitivity of pancreatic cancer cells to these different therapies.
