1.By comparison, most genes have only about 10 exons and are 50 thousand base pairs in length.

相对，多数基因只有10个外显和50kbp长。

2.So what's the variance of an exon?

那么外显的异是多少？机翻

3.Only 50% of BRAF mutations found in NSCLC are V600E (exon 15).

在 NSCLC 中发现的 BRAF 中，只有 50% 是 V600E（外显 15）。机翻

4.Most of these gene mutations are deletions or duplications of one or more exons, and a small amount are point mutations.

基因多数为一个或多个外显的缺失或重复，小部分是点。

5.The most common EGFR-dependent AR mechanism after the T790M mutation in exon 20 is the EGFR C797X point mutation.

20号外显T790M后最常见的EGFR依赖性AR机制是EGFR C797X点。机翻

6.Primary resistance to standard EGFR- TKIs is best and most commonly exemplified by EGFR mutation exon 20 insertions.

对标准 EGFR-TKI 的原发性耐药最好且最常见的例是 EGFR 外显 20 插入。机翻

7.Alright, so the dystrophin gene is a huge gene on the X-chromosome, that has 79 exons and is over 2 million base pairs in length.

抗肌萎缩蛋白基因是X染色体上一个庞的基因，含有79个外显，全长超过2000kbp（书上常缩写为bp，碱基对）。

8.Personalized treatment approaches with MET inhibitors have reported some long-surviving patients with NSCLC harboring a MET exon 14 mutation.

MET 抑制剂的个性化治疗方法已报道了一些携带 MET 外显 14 的长期存活的 NSCLC 患者。机翻

9.Data from this trial prompted FDA approval of tepotinib in MET exon 14-mutant NSCLC.

该试验的数据促使 FDA 批准 tepotinib 用于治疗 MET 外显 14 NSCLC。机翻

10.Mutations sensitive to first-, second- and third-generation EGFR-TKI therapies are classically found in exons 19 (deletion 19) or 21 (single point mutations, L858R).

对第一代、第二代和第三代 EGFR-TKI 疗法敏感的常出现在外显 19（缺失 19）或 21（单点，L858R）中。机翻

11.More base pairs and more exons mean that there are more chances for mistakes during meiosis, which is when the egg or sperm are being created.

更多的碱基对和外显意味着减数分裂时有更多出错的可能，导致生成X染色体上有错误编码序列的卵细胞或者精。

12.A substantial proportion of MET exon 14-mutant NSCLCs express PD-L1 (strong and moderate expression reported in 41% and 22% of cases).

相当比例的 MET 外显 14 NSCLC 表达 PD-L1（据报道，41% 和 22% 的病例有强表达和中度表达）。机翻

13.The gatekeeper T790M mutation in exon 20 of the EGFR gene is the most common mechanism of AR; it is observed in 50- 60% of resistant biopsies.

EGFR基因20号外显的看门人T790M是AR最常见的机制；在 50-60% 的耐药活检中观察到这种情况。机翻

14.MET mutation Both MET exon 14-skipping mutation and MET amplification are primary oncogenic drivers in 3- -5% of patients with NSCLC; MET- dysregulated NSCLCs have a poor prognosis.

MET MET 外显 14 跳跃和 MET 扩增都是 3- -5% NSCLC 患者的主要致癌驱动因素； MET 失调的 NSCLC 预后较差。机翻

15.Mechanisms of AR to MET-TKIs include MET kinase domain mutations and high levels of amplification of the MET exon 14-mutant allele in up to 35% of cases.

AR 至 MET-TKI 的机制包括 MET 激酶结构域和高达 35% 的病例中 MET 外显 14 等位基因的高水平扩增。机翻

16.In contrast to capmatinib, the RR and median PFS with tepotinib did not differ according to treatment line, or the source of MET exon 14 mutation in either tissue or liquid biopsy.

与卡马替尼相比，tepotinib 的 RR 和中位 PFS 并没有因治疗线或组织或液体活检中 MET 外显 14 的源而异。机翻

17.In the PROFILE 1001 trial involving 69 patients with MET exon 14-mutant NSCLC (38% treatment naive), the investigator- reported RR was 32%, with median PFS and OS of 7.3 months and 20.5 months, respectively.

在涉及 69 名 MET 外显 14 NSCLC 患者（38% 未接受过治疗）的 PROFILE 1001 试验中，研究者报告的 RR 为 32%，中位 PFS 和 OS 分别为 7.3 个月和 20.5 个月。机翻

18.12 Amivantamab became the first targeted therapy to be granted FDA approval for patients with EGFR exon 20 insertion NSCLC in May 2021. Similarly, in September 2021, mobocertinib was approved by the FDA in the same setting.

12 Amivantamab 于 2021 年 5 月成为第一个获得 FDA 批准用于治疗 EGFR 外显 20 插入 NSCLC 患者的靶向疗法。同样，2021 年 9 月，mobocertinib 在相同情况下获得 FDA 批准。机翻

19.The most common HER2 mutation, accounting for 80- 90% of all HER2 mutations, occurs in exon 20: a duplication or insertion of the amino acids YVMA at codon 776 (YVMA 776-779 ins).

最常见的 HER2 （占所有 HER2 的 80-90%）发生在外显 20：密码 776 处氨基酸 YVMA 的重复或插入（YVMA 776-779 ins）。机翻

20.No association was noted between the location or type of the MET exon 14 alteration and outcome; however, the occurrence of co-mutations at baseline in PI3KCA (3%), KRAS (2%) or PTEN (3%) correlated with lack of response to tepotinib.

MET 外显 14 改的位置或类型与结果之间没有发现关联；然而，PI3KCA (3%)、KRAS (2%) 或 PTEN (3%) 基线时发生的共与 tepotinib 缺乏反应相关。机翻