• E-mail :[email]
  • Phone : +33 5 61 32 24 04
  • Location : Toulouse, France
Last update 2011-04-04 13:54:37.044

JEROME TORRISANI Genetic and epigenetic alterations in pancreatic and hepatic carcinogenesis

Course and current status


Senior Scientist INSERM


Date of birth: August 4th, 1974

City of birth : Romagnat, France

Marital status: Married, one child

Citizenship: French



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




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 ductal adenocarcinoma (PDAC) and hepatocellular carcinoma (HCC) are the 4th and 5th cause of cancer death in Western countries, respectively. The poor diagnosis of these two digestive cancers requires a better understanding of molecular alterations that occur during their development.

My research focuses on these alterations. More specifically, I am interested in epigenetic alterations that appear early in the development of PDAC and in the role of the DNA methyltransferases (DNMTs) in PDAC initiation. We recently showed that DNA hypermethylation is responsible for the inhibition of miR-148a expression in preneoplastic lesions. We also showed that hypermethylated DNA can serve as a diagnostic marker for PDAC.

In parallel we demonstrated that the transcription factor KLF6 (Krüppel Like Factor) plays an important role in HCC development. Indeed, we and others showed that KLF6 mRNA expression is decreased In HCC samples. More recently, splice variants of KLF6 were described. We demonstrated that the SV2 variant displays anti-apoptotic and antiproliferative functions in hepatic cancer cell lines.   

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