Genetic and molecular epidemiology of adult diffuse glioma

Abstract

Previous glioma classification based primarily on tumour histology resulted in considerable interoberver variability and substantial variation in patient survival within grades. Furthermore, there were few known risk factors for glioma. Discoveries over the past decade have deepened our understanding of the molecular alterations underlying glioma and have led to the identification of numerous heritable genetic risk factors. The advances in glioma molecular characterization reframed our understanding of glioma biology and led the World Health Organization (WHO) to develop a new classification system for glioma. The WHO 2016 classification system comprises five glioma subtypes categorized by both tumour morphology and molecular genetic information, which led to reduced misclassification and more-uniform outcomes within glioma subtypes. To date, 25 risk loci for glioma have been identified and several rare inherited mutations that might cause glioma in some families have been discovered. This Review focuses on the two dominant trends in glioma science: the characterization of diagnostic and prognostic tumour markers and the identification of genetic and non-genetic risk factors. An overview of the many challenges still facing glioma researchers is also included.

Long non-coding RNA NCK1-AS1 promotes the tumorigenesis of glioma through sponging microRNA-138-2-3p and activating the TRIM24/Wnt/β-catenin axis

“…The current clinical treatment of glioma includes surgery, chemotherapy, radiotherapy, targeted therapy and immunotherapy; however, the prognosis of glioma remains unfavorable with a high recurrence rate after initial treatment [2]. Diffuse glioma comprises no more than 1% of all newly diagnosed cancers, though, it leads to high mortality and morbidity, especially the most lethal type, glioblastoma, which takes place with 70-75% of all glioma cases with a median overall survival of 14-17 months [3]. Developing novel therapeutic options and identifying new molecular mechanisms are of great importance in glioma control.…”

Deeping in the Role of the MAP-Kinases Interacting Kinases (MNKs) in Cancer

“…Gliomas are the most common primary brain tumors in adults and arise from the glial tissue. Based on histological criteria, WHO has classified diffuse gliomas into lower-grade astrocytomas or oligodendrogliomas and high-grade astrocytomas, also known as glioblastoma multiforme (GBM), the most prevalent and aggressive type of brain cancer [145]. Clinical studies have demonstrated that there is a higher expression of MNK1 at protein levels in GBM tumor samples and glioma cell lines compared with non-tumorous brain tissue and normal human astrocytes, respectively.…”

Hypoxia-induced lncRNA PDIA3P1 promotes mesenchymal transition via sponging of miR-124-3p in glioma

“…Although treatments including maximal safe resection, radiotherapy, and adjuvant temozolomide have evidently improved the outcomes of glioma patients, they still lag behind those of other tumors 2,3 . Due to the emerging identification of biomarkers which affect the biological features of tumors, glioma genotype can be more informative than histological phenotype in providing a more accurate diagnosis, reliable prognosis, and treatment strategies in early phase trials [4][5][6] .…”