Mutational Strand Asymmetries in Cancer Genomes Reveal Mechanisms of DNA Damage and Repair
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- 作者：Nicholas J. Haradhvala1 ; 2 ; 8 ; Paz Polak1 ; 2 ; 3 ; 8 ; Petar Stojanov4 ; Kyle R. Covington5 ; Eve Shinbrot5 ; Julian M. Hess2 ; Esther Rheinbay1 ; 2 ; Jaegil Kim2 ; Yosef E. Maruvka1 ; 2 ; Lior Z. Braunstein2 ; Atanas Kamburov1 ; 2 ; 3 ; Philip C. Hanawalt6 ; David A. Wheeler5 ; Amnon Koren2 ; 7 ; Michael S. Lawrence2 ; 9 ; lawrence@broadinstitute.org" class="auth_mail" title="E-mail the corresponding author ; Gad Getz1 ; 2 ; 3 ; 9 ; gadgetz@broadinstitute.org" class="auth_mail" title="E-mail the corresponding author
- 刊名：Cell
- 出版年：2016
- 出版时间：28 January 2016
- 年：2016
- 卷：164
- 期：3
- 页码：538-549
- 全文大小：1962 K
文摘
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Replicative and transcriptional mutational asymmetries are widespread across cancer
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APOBEC mutagenesis in humans primarily occurs on the lagging-strand template
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Mismatch repair balances asymmetric replication errors
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Transcription-coupled damage (TCD) introduces sense-strand mutations in liver cancer