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线粒体突变促使前列腺癌入侵作者：Jan Korbel, Thorsten Schlomm, Robert G. Bristow 众所周知，核基因突变能促进肿瘤的发生、侵袭和对治疗的反应。相反，在母系遗传的线粒体基因组中，突变的频率和作用，我们了解甚少。我们对384个限性前列腺癌患者的线粒体基因组进行测序，并确定了每个病人一个线粒体单核苷酸变异（mtsnv）的中位数。部分这些mtsnvs发生在复发性突变热点，并伴随侵袭性疾病。跟年纪大的相比，年轻的患者有较少的mtsnvs。我们展示了线粒体和核突变结构之间的紧密联系，在特定突变之间同时发生。例如，某些控制区mtsnvs同时发生，获得致癌基因MYC，而这些突变与患者生存率相关。这些数据表明前列腺癌中线粒体突变频繁，并提示前列腺癌中线粒体和线粒体突变结构之间的相互作用。
Panorama of mitochondrial mutations in prostate cancer. a The top panel displays the number of mtSNVs per patient sorted first by T-Category and then by the number of mtSNVs; histogram bars are colored by the average difference in the heteroplasmy fraction (∆HF) between tumor and normal samples, light-blue 20–40%, medium-blue 40–60%, dark-blue ≥60%. A heatmap showing the location of each mtSNV on the mitochondrial genome (middle), where the color of each dot represents ∆HF. The mitochondrial genome is represented on the left. The bottom panel shows the clinical covariates for all 384 patients: Age, Gleason Score, PSA, and T-Category. Bottom right: Associations between the covariates and number of mtSNVs. b Frequency and distribution of single-nucleotide variants (SNVs) within the mitochondrial genome. Mutation frequency normalized by dividing the number of mutations per locus of each patient by (length of the locus (kbp) × MCN). c Distribution of mtSNVs across the mitochondrial genome. mtSNVs were fairly evenly distributed across the genome (black bars) and recurrent mutation positions are indicated by the histogram 原文阅读 https://www.nature.com/articles/s41467-017-00377-y 相关阅读 线粒体酶CLPP缺失保护小鼠免受饮食诱导的肥胖和胰岛素抵抗 Magigen T7核酸内切酶I / T7 Endonuclease I Magigen耐高温RNase HII-核糖核酸酶 - rhPCR好帮手！ Magigen Bst DNA聚合酶 - 与环介导恒温扩增LAMP技术完美结合 Magigen LAMP试剂盒 - 环介导恒温扩增技术典范 Magigen一步法RT-qPCR预混液试剂盒-轻松搞定反转录qPCR |
