Abstract
Background: Epigenetic changes play crucial roles in cancer initiation and progression and in tumor recurrence. Glioblastoma multiforme (GBM) is by far the most common and most malignant of the glial tumors, and its recurrence is ineluctable. Thus, anti-GBM therapy need for new treatments for recurrent GBM. We here in focused on identifying whether TET2 (an epigenetic players involving in the DNA demethylation process) as a putative target for the development of anti-GBM therapy. Results: We observed that the expression level of TET2 at mRNA and protein levels is not associated with a prognosis value of survival in GBM patients. However, in a cohort of 10 GBM patients having received two surgical resections (rGBM), we noted that three in ten rGBM patients have an increase of TET2 expression between resection#1 and #2. Conclusions: By observing an increase of TET2 expression between two surgical resections an despite the fact that expression level of TET2 is devoid of prognosis value of survival in GBM patients, our data provide a promising starting point for the use of TET2 inhibitors administrable in the subgroup of patients with recurrent GBM.
Highlights
The Ten-Eleven Translocation-2 (TET2) is a member of the TET family proteins that include 2 other members: TET1 and TET3
By observing an increase of TET2 expression between two surgical resections an despite the fact that expression level of TET2 is devoid of prognosis value of survival in Glioblastoma multiforme (GBM) patients, our data provide a promising starting point for the use of TET2 inhibitors administrable in the subgroup of patients with recurrent GBM
We observed that the expression level of TET2mRNA in GBM is not associated with a prognosis value of survival, neither in term of overall survival (OS) (Figure 1)
Summary
The Ten-Eleven Translocation-2 (TET2) is a member of the TET family proteins that include 2 other members: TET1 and TET3. These proteins catalyze the steps of the active DNA cytosinedemethylation via the conversion of 5-methylcytoisne (5mC) to 5-hydroxymethylcytosine (5hmC), 5-formylcytosine (5fC) and 5-carboxycytosine (5CaC) [1,2,3]. Epigenetic changes play crucial roles in cancer initiation and progression and in tumor recurrence. Anti-GBM therapy need for new treatments for recurrent GBM. We here in focused on identifying whether TET2 (an epigenetic players involving in the DNA demethylation process) as a putative target for the development of anti-GBM therapy
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