Noel Raynal

Education

• Post-doctoral fellow at MD Anderson Cancer Center, Department of Leukemia, University of Texas, Houston, TX, and Fels Institute for Cancer Research and Molecular Biology, Temple University, Philadelphia, PA, É.-U., 2009-2013
• Ph.D. in biology, INRS-Institut Armand-Frappier, 2003-2008
• M.Sc. in biology, Département des Sciences Biologiques, Université du Québec à Montréal, 2001-2003

Research Interests

Epigenomics refer to molecular mechanisms that orchestrate gene expression and cellular phenotype without any alteration in DNA sequence. These modifications, such as DNA methylation, histone acetylation and methylation are strongly altered in pediatric cancers. Many tumor suppressor genes are silenced in cancer due to DNA hypermethylation and/or histone deacetylation. 

Epigenetic therapy targets epigenomic alterations aiming to reprogram cancer cells, to trigger cell differentiation and inhibit cell proliferation. Epidrugs of the class of DNA methylation inhibitors or histone deacetylase inhibitors reactivate silenced tumor suppressor genes and block cancer growth. Epidrugs are effective against certain type of adult leukemia and are better tolerated than cytotoxic drugs.

Our long-term goal is to better understand epigenetic modifications in pediatric cancers and to develop targeted epigenetic therapies to improve therapeutic efficacy in hemato-oncology.

Epigenomic alterations in pediatric cancers
Using pediatric cancer cell lines and patient samples, our aim is to better characterize epigenomic alteration at DNA methylation and chromatin levels of specific loci such as genes involved in cellular differentiation. We will assess the contribution of these changes to better understand the cancer cell biology. 

Targeted therapy using combinations of epigenetic drugs against pediatric cancers
Pediatric cancers like leukemia are characterized by several mutations in genes involved in several epigenetic pathways. These alterations trigger epigenomic modifications that represent potential targets to improve the treatment of pediatric cancers. We use drug screening platforms to discover new epigenetic drugs using different cell culture models and drug libraries. 

Our laboratory has a core expertise in molecular biology and cell culture to tackle these important questions in cancer epigenetics and drug development. Our laboratory emphasizes teamwork and communication to create a dynamic and exciting workplace ideal for students and post-doctoral fellows.

Awards and Distinctions

• Transition grant, Cole Foundation, 2013-2016

Publications

Raynal NJ-M, Si J, Taby RF, Gharibyan V, Ahmed S, Jelinek J, Estécio MR, Issa JP, 
DNA methylation does not stably lock gene expression but instead serves as a molecular mark for gene silencing memory
Cancer Res 2012  1170-1181.

Raynal NJ-M, Momparler LF, Rivard G-É, Momparler RL, 
3-deazauridine enhances the antileukemic action of 5-aza-2′-deoxycytidine and targets drug-resistance due to deficiency in deoxycytidine kinase
Leukemia Res 2011  110-118.

Spannhoff A, Kim Y, Raynal NJ-M, Gharibyan V, Su MB, Zhou Y, Castellano S, Sbardella G, Issa JP, Bedford MT, 
Histone deacetylase inhibitor activity in royal jelly might facilitate caste switching in bees
EMBO Rep 2011  238-243.

Raynal NJ-M, Momparler LF, Charbonneau M, Momparler RL, 
Synergistic effect of 5-Aza-2′-deoxycytidine and genistein in combination against leukemia.
Oncol Res 2008  223-230.

Raynal NJ-M, Momparler LF, Charbonneau M, Momparler RL, 
Antileukemic activity of genistein, a major isoflavone present in soy products
J Nat Prod 2008  3-7.