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Waddell et al performed whole-genome sequencing and copy number variation analysis, including analysis for widespread and complex patterns of chromosomal rearrangement, in 100 PDACs. Chromosomal rearrangements leading to gene disruption were prevalent, affecting genes known to be important in pancreatic cancer (TP53,SMAD4, CDKN2A, ARID1A, and ROBO2) and new candidate drivers of pancreatic carcinogenesis (KDM6A and PREX2). A significant proportion harbored focal amplifications, many of which contained druggable oncogenes (ERBB2, MET, FGFR1, CDK6, PIK3R3, and PIK3CA), but at low prevalence in individual patients. Genomic instability co-segregated with inactivation of DNA maintenance genes (BRCA1, BRCA2, or PALB2) and a mutational signature of DNA damage repair deficiency. Based on structural variation profiles, PDACs were classified into four subtypes based on predominant genetic alterations with different clinical outcomes, including stable, locally rearranged, scattered, and unstable. The ‘stable’ subtype contains ≤ 50 structural variation events and often exhibits widespread aneuploidy, suggesting the presence of defects in cell cycle regulation. The ‘locally rearranged’ subtype contains a copy number gain that harbors known oncogenes. Known oncogenes include common focal amplifications in KRAS, SOX9, and GATA6 and potential therapeutic targets such as ERBB2, MET, CDK6, PIK3CA,and PIK3R3. The remaining genetic alterations in the ‘locally rearranged’ subtype involve complex genomic events such as breakage–fusion–bridges or chromothripsis, which is linked to TP53 mutations in medullobastoma and acute myeloid leukemia. The scattered class exhibit a moderate level of non-random chromosomal damage and 50–200 structural variation events. The ‘unstable’ subtype has defects in maintaining DNA integrity and could be sensitive to DNA-damaging agents. A platinum-containing combination therapy is emerging as a treatment option for advanced PDAC. Defining biomarkers of platinum responsiveness would significantly alter current treatment approaches to PDAC and improve overall outcomes. The researchers defined biomarkers, based on a combination of changes in gene structure, genetic mutations, and mutation features, that characterize the effectiveness of this treatment method. In a series of 8 patients who received platinum-based chemotherapy, of the 5 patients with unstable genomes and/or a high BRCA mutational signature burden, 2 had exceptional responses (defined as complete radiological resolution of disease and normalization of CA19.9 levels), and 2 had robust partial responses based on RECIST 1.1 criteria. None of the 3 patients without an ‘unstable’ genome showed a response. These results support the efficacy of individual tumor therapy。
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Waddell et al performed whole-genome sequencing and copy number variation analysis, including analysis for widespread and complex patterns of chromosomal rearrangement, in 100 PDACs. Waddell等人在100例 PDACs中（Pancreatic ductal adenocarcinomas？？胰腺导管腺癌？？）进行了全基因组序列和拷贝数变异分析，包括分析染色体重排的广泛复杂模式。Chromosomal rearrangements leading to gene disruption were prevalent, affecting genes known to be important in pancreatic cancer (TP53,SMAD4, CDKN2A, ARID1A, and ROBO2) and new candidate drivers of pancreatic carcinogenesis (KDM6A and PREX2). 染色体重排导致基因中断是广泛存在的，进而影响已知对胰腺癌具有重要意义的基因表达(TP53,SMAD4, CDKN2A, ARID1A, and ROBO2)和胰腺肿瘤新候选的驱动基因表达(KDM6A and PREX2)。A significant proportion harbored focal amplifications, many of which contained druggable oncogenes (ERBB2, MET, FGFR1, CDK6, PIK3R3, and PIK3CA), but at low prevalence in individual patients. 局部扩增的基因占重要的比例，包括许多成药致癌基因 (ERBB2, MET, FGFR1, CDK6, PIK3R3, and PIK3CA)，但是在个别患者中发生率低。Genomic instability co-segregated with inactivation of DNA maintenance genes (BRCA1, BRCA2, or PALB2) and a mutational signature of DNA damage repair deficiency. 基因不稳定性与DNA修复基因失活以及DNA损伤修复缺陷的突变签名(BRCA1, BRCA2, or PALB2)存在共分离。Based on structural variation profiles, PDACs were classified into four subtypes based on predominant genetic alterations with different clinical outcomes, including stable, locally rearranged, scattered, and unstable.根据结构变异的特征，PDACs 以不同临床结局的优势基因突变为依据，分为四种亚型，包括稳定型、局部基因重排型、基因断裂型及不稳定型。The ‘stable’ subtype contains ≤ 50 structural variation events and often exhibits widespread aneuploidy, suggesting the presence of defects in cell cycle regulation. 稳定型包含小于等于50个结构变异事件，并常表现为广泛的非整倍性，这提示在细胞周期调控中存在缺陷。The ‘locally rearranged’ subtype contains a copy number gain that harbors known oncogenes. 局部重排型包含一个拷贝数增益，包含已知的致癌基因。Known oncogenes include common focal amplifications in KRAS, SOX9, and GATA6 and potential therapeutic targets such as ERBB2, MET, CDK6, PIK3CA,and PIK3R3. 已知的致癌基因包括常见局部扩增的KRAS, SOX9, 和 GATA6以及潜在治疗的靶基因，如ERBB2, MET, CDK6, PIK3CA和PIK3R3。The remaining genetic alterations in the ‘locally rearranged’ subtype involve complex genomic events such as breakage–fusion–bridges or chromothripsis, which is linked to TP53 mutations in medullobastoma and acute myeloid leukemia. 局部重排型中剩余的基因突变包括复杂基因组事件，如基因断裂-融合-桥接或者染色体碎裂，这与medullobastoma（这个单词貌似有误，应该是medulloblastoma,成神经管细胞瘤）和急性髓系白血病的TP53突变有关联。The scattered class exhibit a moderate level of non-random chromosomal damage and 50–200 structural variation events. 基因断裂型表现为中等水平的非随机性染色体损伤和50到200个结构突变事件。The ‘unstable’ subtype has defects in maintaining DNA integrity and could be sensitive to DNA-damaging agents. 不稳定型在维持DNA完整性中有缺陷，并对DNA损伤试剂敏感。A platinum-containing combination therapy is emerging as a treatment option for advanced PDAC. 含铂类药物联合治疗将成为进展期PDAC的一个治疗选择。Defining biomarkers of platinum responsiveness would significantly alter current treatment approaches to PDAC and improve overall outcomes.明确铂类药物反应性生物标记物将显著性改变目前PDAC的治疗方案，并改善总体的疗效。 The researchers defined biomarkers, based on a combination of changes in gene structure, genetic mutations, and mutation features, that characterize the effectiveness of this treatment method.研究者根据基因结构改变、基因突变和突变特征的联合评估来明确这些生物标记物，并具有使这个治疗方法有效的特点。In a series of 8 patients who received platinum-based chemotherapy, of the 5 patients with unstable genomes and/or a high BRCA mutational signature burden, 2 had exceptional responses (defined as complete radiological resolution of disease and normalization of CA19.9 levels), and 2 had robust partial responses based on RECIST 1.1 criteria. 在一系列接受铂类药物基础化疗的8个患者中，根据RECIST 1.1标准，有5个患者表现为不稳定型基因组和/或高BRCA突变签名负荷，有2个患者表现为异常性反应（定义为疾病的完全放射分辨率和CA19.9水平正常化）以及有2个患者表现为强烈的部分反应。None of the 3 patients without an ‘unstable’ genome showed a response.没有不稳定型基因组的 3个患者都表现为没有反应性。These results support the efficacy of individual tumor therapy。这些结果证明肿瘤个体化治疗具有疗效。
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可以用google翻译输入查询，然后适当修改下即可。以下是我用google翻译翻译的。Waddell等人在100个PDAC中进行全基因组测序和拷贝数变异分析，包括广泛和复杂的染色体重排模式的分析。导致基因破坏的染色体重排是普遍的，影响已知在胰腺癌（TP53，SMAD4，CDKN2A，ARID1A和ROBO2）中已知重要的基因和胰腺癌发生的新候选驱动因子（KDM6A和PREX2）。大部分病灶扩大，其中许多包含药物致癌基因（ERBB2，MET，FGFR1，CDK6，PIK3R3和PIK3CA），但个体患者的流行率较低。基因组不稳定性与DNA维持基因（BRCA1，BRCA2或PALB2）的失活共同分离，DNA损伤修复缺陷的突变特征。基于结构变异特征，根据具有不同临床结果的主要遗传改变，将PDAC分为四个亚型，包括稳定的，局部重排的，分散的和不稳定的。 “稳定”亚型包含≤50个结构变异事件，并且通常表现出广泛的非整倍性，表明细胞周期调节中存在缺陷。 “本地重排”子类型包含拥有已知致癌基因的拷贝数增益。已知的致癌基因包括KRAS，SOX9和GATA6中的常见放大和可能的治疗靶标，如ERBB2，MET，CDK6，PIK3CA和PIK3R3。 “局部重排”亚型中剩余的遗传改变涉及复杂的基因组事件，例如断裂融合桥或染色体错构，其与髓母细胞瘤和急性骨髓性白血病中的TP53突变相关。
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求大神翻译,中国古体字
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