ENAapplication/xmlftp://ftp.sra.ebi.ac.uk/vol1/fastq/DRR040/DRR040697/DRR040697.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/DRR040/DRR040702/DRR040702.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/DRR040/DRR040698/DRR040698.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/DRR040/DRR040703/DRR040703.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/DRR040/DRR040699/DRR040699.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/DRR040/DRR040701/DRR040701.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/DRR040/DRR040700/DRR040700.fastq.gzprimary200OKGenomicsGastroenterology and Hepatology, Graduate School of Medicine, Kyoto Universityhttps://www.ebi.ac.uk/ena/browser/view/PRJDB4076Mus musculusTo unveil the mutation signature accumulated in the tumors developed in the liver with MSH2 deficiency and/or AID up-regulation, we performed whole-exome sequencing of 6 independent HCCs from ALB-MSH2-/-, ALB-AID, and ALB-MSH2-/--AID mice. As a control, we also determined the whole-exome sequences of the liver of ALB-Cre.ENAfalseMus musculusThe exome sequences of HCCs developed in ALB-MSH2-/-, ALB-AID, and ALB-MSH2-/-AID mice.2025-09-242017-07-30PRJDB407610090