Hanane BAIDARJAD

Roles of NEIL3 DNA glycosylase in glioblastoma telomere dynamics: From molecular insights to preclinical target validation
There is no cure for glioblastoma (GBM), the most aggressive and lethal primary brain tumor. Cancer cells must activate mechanisms to maintain telomeres, the physical ends of our chromosomes, in order to acquire limitless replicative potential. Although targeting DNA repair and telomere maintenance mechanisms have emerged as important therapeutic strategies for many cancers, identifying suitable targets for such strategies in GBM remains a considerable challenge.
Telomeres need special protection from oxidative DNA damage – an inevitable consequence of cellular metabolism. Involved in the removal of oxidized guanines in telomeric DNA is the DNA repair protein NEIL3. We have shown that NEIL3 is required for telomere protection and chemoresistance in GBM cells, suggesting that it represents a relevant therapeutic target in GBM. Our experiments may pave the way for novel DNA repair-based strategies against GBM.
Our objectives are to understand the molecular mechanisms whereby NEIL3 regulates telomere dynamics in adult and pediatric GBM. Our experiments may pave the way for novel DNA repair-based strategies against GBM.

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