CV Science

Mélanie Barthelemy Lab Engineer

Course and current status

- Since 2011: Lab Engineer at Centre Jean Perrin in CREaT team. Characterization of the response of normal human brain tissue and tumor to anti-glioma treatment. Centre Jean Perrin, Clermont-Ferrand, FRANCE.

- 2009-2011: lab Engineer at Curie Institut during 24 months on Biophenics Platform. Establishment of high-contents screening conditions by imaging of siRNA libraries to identify new targets for use in oncology. Institut Curie, Paris, FRANCE.

- 2008-2009: lab Technician for collaboration between Servier and Curie Instituts for 18 months on Biophenics Platform. Studying of genes involved in the survival of lung cancer cells in order to identify new therapeutic targets by phenotypic screening. Institut Curie, Paris, FRANCE.

2005-2007: Professional Master (French equivalent of Master degree), Cellular and Molecular Biology, Lille 1, FRANCE.

To validate my degree I did an intership in Merck-Serono Laboratories during 6 month. My project was to develop molecular tools for identify molecular targets in type 2 diabetes.

2005: Bachelor degree in cellular biology and physiology, Lille 1, FRANCE

2002-2004: Academic and Technologic Degree, Biological and Biochemical Analysis, Lille 1, FRANCE.

To validate my degree I did an intership in the Collaborative Research for Effective Diagnostic (CRED) at Sherbrook in Canada. I had to develop a method for the determination of salivary testosterone and then to compare with the bioavailable testosterone .

Scientific summary

Glioblastoma is the central nervous system tumors the most common and most aggressive. Classically, these tumors are treated with surgery and radiotherapy with chemotherapy. Despite the benefits of radiotherapy remains a standard treatment, the median patient survival is less than 14 months, mostly due to a recurrence even within the irradiated volume. The failure of current treatments require necessary to identify and validate new therapeutic targets. Understanding the biological mechanisms of radioresistance causing recidivism leaves hope for the emergence of new therapeutic targets whose neutralization associated with a high precision spatial targeting of irradiation could improve the antitumor efficacy without increase toxicity. Cell response to irradiation may be considered the result of two mechanisms: intrinsic radioresistance linked to the tumor cell itself, and the influence of interactions between the tumor and its microenvironment.

The study of signaling pathways in these tumors identified several therapeutic targets, including the potential role of interleukin-6 (IL-6) in the anti-apoptotic mechanisms involved in radioresistance. Indeed, IL-6 activates STAT3 protein by phosphorylating the Y705 residue, which therefore makes this protein of a potential therapeutic target. But it was shown that the protein can also be phosphorylated STAT3, independently of IL-6, another residue (Serine 727) with biological consequences are still poorly understood, but could explain the phenomen of tolerance to the inhibition of IL-6/gp130/STAT3 towards maintaining activation of STAT3 sufficient to induce the target genes. Protein kinase C epsilon (PKCe), highly expressed in brain tumors has been recently described as responsible for the phosphorylation of serine 727 of STAT3. One goal of the laboratory is to explore the possible role of phosphorylation of serine 727 of STAT3 in the intrinsic radioresistance of glioblastoma.