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Mutational signatures reveal the dynamic interplay of risk factors and cellular processes during liver tumorigenesis |pdf=|usr=}}{{29101368 }} gab.com Text Mutational signatures reveal the dynamic interplay of risk factors and cellular processes during liver tumorigenesis JO: Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=29101368 #FOAvip Genomic alterations driving tumorigenesis result from the interaction of environmental exposures and endogenous cellular processes. With a diversity of risk factors, liver cancer is an ideal model to study these interactions. Here, we analyze the whole genomes of 44 new and 264 published liver cancers and we identify 10 mutational and 6 structural rearrangement signatures showing distinct relationships with environmental exposures, replication, transcription, and driver genes. The liver cancer-specific signature 16, associated with alcohol, displays a unique feature of transcription-coupled damage and is the main source of CTNNB1 mutations. Flood of insertions/deletions (indels) are identified in very highly expressed hepato-specific genes, likely resulting from replication-transcription collisions. Reconstruction of sub-clonal architecture reveals mutational signature evolution during tumor development exemplified by the vanishing of aflatoxin B1 signature in African migrants. Finally, chromosome duplications occur late and may represent rate-limiting events in tumorigenesis. These findings shed new light on the natural history of liver cancers. Twit Text FOAVip Mutational signatures reveal the dynamic interplay of risk factors and cellular processes during liver tumorigenesis ????Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=29101368 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29101368 #FOAvip English Wikipedia <ref>{{Cite pmid|29101368 }}</ref> Mutational signatures reveal the dynamic interplay of risk factors and cellular processes during liver tumorigenesis #MMPMID29101368 Letouzé E ; Shinde J ; Renault V ; Couchy G ; Blanc JF ; Tubacher E ; Bayard Q ; Bacq D ; Meyer V ; Semhoun J ; Bioulac-Sage P ; Prévôt S ; Azoulay D ; Paradis V ; Imbeaud S ; Deleuze JF ; Zucman-Rossi J Nat Commun 2017[Nov]; 8 (1 ): 1315 PMID29101368 show ga Genomic alterations driving tumorigenesis result from the interaction of environmental exposures and endogenous cellular processes. With a diversity of risk factors, liver cancer is an ideal model to study these interactions. Here, we analyze the whole genomes of 44 new and 264 published liver cancers and we identify 10 mutational and 6 structural rearrangement signatures showing distinct relationships with environmental exposures, replication, transcription, and driver genes. The liver cancer-specific signature 16, associated with alcohol, displays a unique feature of transcription-coupled damage and is the main source of CTNNB1 mutations. Flood of insertions/deletions (indels) are identified in very highly expressed hepato-specific genes, likely resulting from replication-transcription collisions. Reconstruction of sub-clonal architecture reveals mutational signature evolution during tumor development exemplified by the vanishing of aflatoxin B1 signature in African migrants. Finally, chromosome duplications occur late and may represent rate-limiting events in tumorigenesis. These findings shed new light on the natural history of liver cancers. |*Mutation [MESH] |Carcinogenesis/*genetics [MESH] |Carcinoma, Hepatocellular/etiology/*genetics [MESH] |Chromosome Duplication [MESH] |DNA Mutational Analysis [MESH] |DNA Replication [MESH] |Evolution, Molecular [MESH] |Female [MESH] |Gene Dosage [MESH] |Gene Rearrangement [MESH] |Genome, Human [MESH] |Humans [MESH] |INDEL Mutation [MESH] |Liver Neoplasms/etiology/*genetics [MESH] |Male [MESH] |Risk Factors [MESH] |Transcription, Genetic [MESH]Mutational signatures reveal the dynamic interplay of risk factors and(epmc).pdf DeepDyve Pubget Overpricing