Whole Genome Sequencing of Liver Cancers
Genomic alterations driving tumorigenesis result from the interaction of environmental exposures and endogeneous cellular processes. With a diversity of risk factors including viral infection, carcinogenic exposures and metabolic diseases, liver cancer is an ideal model to study these interactions. Whole genome sequencing of liver tumors identified 10 mutational signatures showing distinct relationships with environmental exposures, replication and transcription. Transcription-coupled damage was specifically associated with the liver-specific signature 16 and alcohol intake. Flood of indels were identified in very highly expressed hepato-specific genes, likely resulting from replication-transcription collisions. Reconstruction of sub-clonal architecture revealed mutational signature evolution during tumor development exemplified by the vanishing of aflatoxin-B1 signature in African migrants. These findings shed new light on the natural history of liver cancers
- Type: Other
- Archiver: EGA European Genome-Phenome Archive
Click on a Dataset ID in the table below to learn more, and to find out who to contact about access to these data
|EGAD00001003281||Illumina HiSeq 2000||52|
Mutational signatures reveal the dynamic interplay of risk factors and cellular processes during liver tumorigenesis.
Nat Commun 8: 2017 1315
Advances in genomic hepatocellular carcinoma research.
Gigascience 7: 2018 None
Cyclin A2/E1 activation defines a hepatocellular carcinoma subclass with a rearrangement signature of replication stress.
Nat Commun 9: 2018 5235
Hepatitis B virus integrations promote local and distant oncogenic driver alterations in hepatocellular carcinoma.
Gut 71: 2022 616-626