Background

Glioblastoma multiforme is the most frequent and aggressive type of primary brain tumour, which plays an essential role in causing morbidity and mortality in adults. The clinical hallmarks are characterized as its aggressive growth and inexorable recurrence even though the patients may be treated with multimodal therapy with surgery followed combinational chemotherapy and radiation therapy. The average survival time for patients is less than one-year after current standard therapies. Both genetic and epigenetic effects make contributions to the development of human glioblastoma. Recently, a range of studies have reported that epigenetic modifications are involved in the incidence of glioblastomas and that environmental cues may be responsible for the initiation of some forms. A deeper understanding of the epigenetic alterations occurring in glioblastoma could help improve the knowledge relevant to the new biomarkers discovery, tumorigenesis, progression and recurrence of this cancer disease, especially, potential epigenetic therapy for glioblastoma may be validated.This page has no content yet.

Project Objectives

The aim of this study is to investigate the regulatory networks of human glioblastomas to assess the likelihood of an epigenetic or gnetic trigger as the first event in causing brain tumorogenesis. I will generate mRNA-seq and sRNA-seq libraries for Next-Generation sequencing for existing human primary brain tumour samples. Multiple samples from the tumour and neighbouring healthy brain tissues will be analysed to obtain an overview of prominent network features. In particular, it is going tol determine the extent of differential gene expression between healthy brain and tumour tissues for each individual and the degree of variation in differential gene expression between individuals. Once gene networks miss-regulated in brain cancer are identified, the student will assess overrepresented GO-terms, analyse promoter motifs and correlations with epigenetic features. This analysis will generate a working model for epigenetic network regulation in glioblastomas that could be tested in available tumorogenic cell lines.