Transcriptomic Landscape of Lower Grade Glioma Based on Age-Related Non-Silent Somatic Mutations
Glioma accounts for 80% of all malignant brain tumours and is the most common adult primary brain tumour. Age is an important factor affecting the development of cancer, as somatic mutations accumulate with age. Here, we aimed to analyse the significance of age-dependent non-silent somatic mutations...
Main Authors: | , , , , , , , , , |
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Format: | Article |
Language: | English |
Published: |
MDPI AG
2021-06-01
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Series: | Current Oncology |
Subjects: | |
Online Access: | https://www.mdpi.com/1718-7729/28/3/210 |
Summary: | Glioma accounts for 80% of all malignant brain tumours and is the most common adult primary brain tumour. Age is an important factor affecting the development of cancer, as somatic mutations accumulate with age. Here, we aimed to analyse the significance of age-dependent non-silent somatic mutations in glioma prognosis. Histological tumour grade depends on age at diagnosis in patients with <i>IDH1</i>, <i>TP53</i>, <i>ATRX</i>, and <i>EGFR</i> mutations. Age of patients with wild-type <i>IDH1</i> and <i>EGFR</i> increased with increase in tumour grade, while the age of patients with <i>IDH1</i> or <i>EGFR</i> mutation remained constant. However, the age of patients with <i>EGFR</i> mutation was higher than that of patients with <i>IDH1</i> mutation. The hierarchical clustering of patients was dominantly separated by <i>IDH1</i> and <i>EGFR</i> mutations. Furthermore, patients with <i>IDH1</i> mutation were dominantly separated by <i>TP53</i> and <i>ATRX</i> double mutation and its double wild-type counterpart. The age of patients with <i>ATRX</i> and <i>TP53</i> mutation was lower than that of patients with wild-type <i>ATRX</i> and <i>TP53</i>. Patients with the double mutation showed poorer prognosis than those with the double wild type genotype. Unlike <i>IDH1</i> mutant, <i>IDH1</i> wild-type showed upregulation of expression of epithelial mesenchymal transition associated genes. |
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ISSN: | 1198-0052 1718-7729 |