Non-Mendalian inheritance of extrachromosal DNA elements can drive disease evolution in glioblastoma

Study ID Alternative Stable ID Type
EGAS00001001878 Other

Study Description

Genomic heterogeneity of glioblastoma (GBM) is suspected to contribute to the poor response to therapy of this disease. We compared molecular characteristics between primary GBM, neurospheres and orthotopic xenograft models derived from the same parental tumor. Driver alterations were in majority propagated from tumor to model systems. Extrachromosomal amplifications of MET, a proto-oncogene coding for a receptor tyrosine kinase, were detected in three primary GBM, largely discarded in neurospheres cultures, but resurfaced in xenografts. The clonal dynamics inferred by somatic single nucleotide variants (sSNVs) in MET-amplified samples diverged from the pattern delineated by the MET amplification event suggesting that the MET event and sSNVs were inherited in different manners. Our analysis shows that extrachromosomal elements are able to drive tumor progression.

Study Datasets 4 datasets.

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Dataset ID Description Technology Samples
Whole transcriptome sequencing generated from patient, neurosphere and xenograft samples
Illumina HiSeq 2000 64
Whole exome sequencing generated from 13 sets of patient, neurosphere and xenograft samples
Illumina HiSeq 2000 82
This data set consists of 82 whole genome low pass sequencing bams used in HF-GBM-Tumor-Neurosphere-Xenograft
Illumina HiSeq 2000 82
This data set consists of whole genome SMRT sequencing fastqs generated from 2 xenograft samples.
PacBio RS II 2

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