Whole Genomes Define Concordance in Matched Primary, Xenograft, and Organoid Models of Pancreas Cancer
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Pancreatic ductal adenocarcinoma (PDAC) has the worst prognosis of any common solid epithelial tumour. Multiple failed clinical trials necessitate newer approaches to understand the molecular etiology of this disease. Patient-derived xenografts (PDX) and patient-derived organoids (PDO) may serve as pre-clinical disease models; however, characterization remains largely unaddressed at the whole genome level. We conducted a comprehensive assessment of the genetic landscape of tumours and matched PDX and PDO from patients with PDAC. Our data show that PDX and PDO recapitulate PDAC tumourigenesis with respect to simple somatic mutations and copy number changes, and capture major structural variation events.
Study Datasets 4 datasets.
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Whole Genomes Define Concordance in Matched Primary, Xenograft, and Organoid Models of Pancreas Cancer - WGS mapped reads
Bam files from WGS of PDAC samples described in: Transcription phenotypes of pancreatic cancer are driven by genomic events events during tumour evolution
Bam files from WGS of PDAC samples used in the PCSI mismatch repair study
Background and Aims: Homologous recombination deficiency (HRD) in pancreatic ductal adenocarcinoma (PDAC), remains poorly defined beyond germline(g) alterations in BRCA1, BRCA2 and PALB2. Methods: We interrogated whole genome sequencing (WGS) data on 391 patients including 49 carriers of pathogenic variants (PVs) in g_BRCA_ and PALB2. HRD classifiers were applied to the dataset and included: 1) the genomic instability score (GIS) used by Myriad MyChoice HRD assay; 2) substitution base signature ... (Show More)
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