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Cancer mutational burden is shaped by G4 DNA, replication stress and mitochondrial dysfunction
A hallmark of cancer is genomic instability, which can enable cancer cells to evade therapeutic strategies. Here we employed a computational approach to uncover mechanisms underlying cancer mutational burden by focusing upon relationships between 1) translocation breakpoints and the thousands of G4...
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| 出版年: | Prog Biophys Mol Biol |
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| 主要な著者: | , , , |
| フォーマット: | Artigo |
| 言語: | Inglês |
| 出版事項: |
2019
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| 主題: | |
| オンライン・アクセス: | https://ncbi.nlm.nih.gov/pmc/articles/PMC6745008/ https://ncbi.nlm.nih.gov/pubmed/30880007 https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1016/j.pbiomolbio.2019.03.004 |
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