Gliosarcoma: The Distinct Genomic Alterations Identified by Comprehensive Analysis of Copy Number Variations.
Chuan-Dong ChengCheng ChenLi WangYong-Fei DongYang YangYi-Nan ChenWan-Xiang NiuWen-Chao WangQing-Song LiuChao-Shi NiuPublished in: Analytical cellular pathology (Amsterdam) (2022)
Gliosarcoma (GSM), a histologic variant of glioblastoma (GBM), carries a poor prognosis with less than one year of median survival. Though GSM is similar with GBM in most clinical and pathological symptoms, GBM has unique molecular and histological features. However, as the rarity of GSM samples, the genetic information of this tumor is still lacking. Here, we take a comprehensive analysis of DNA copy number variations (CNV) in GBM and GSM. Whole genome sequencing was performed on 21 cases of GBM and 15 cases of GSM. CNVKIT is used for CNV calling. Our data showed that chromosomes 7, 8, 9, and 10 were the regions where CNV frequently happened in both GBM and GSM. There was a distinct CNV signal in chromosome 2 especially in GSM. The pathway enrichment of genes with CNV was suggested that the GBM and GSM shared the similar mechanism of tumor development. However, the CNV of some screened genes displayed a disparate form between GBM and GSM, such as AMP, BEND2, HDAC6, FOXP3, ZBTB33, TFE3, and VEGFD. It meant that GSM was a distinct subgroup possessing typical biomarkers. The pathways and copy number alterations detected in this study may represent key drivers in gliosarcoma oncogenesis and may provide a starting point toward targeted oncologic analysis with therapeutic potential.
Keyphrases
- copy number
- mitochondrial dna
- genome wide
- poor prognosis
- dna methylation
- long non coding rna
- prostate cancer
- healthcare
- clinical trial
- immune response
- dendritic cells
- depressive symptoms
- drug delivery
- regulatory t cells
- big data
- cancer therapy
- genome wide identification
- minimally invasive
- deep learning
- study protocol
- nucleic acid