1.There are so called oncogenic or tumor producing genes.

有所谓致癌或产生肿因。

2.Approximately 50% of advanced NSCLCs have a known oncogenic alteration (Figure 7.1).

大约 50% 晚期 NSCLC 有已知致癌改变（图 7.1）。机翻

3.Oncogenic NTRK can fuse with several partners and is an emerging therapeutic target in several pediatric and adult solid tumors.

致癌性 NTRK 可以与多种伙伴融合，是多种儿童和成人实体新兴治疗靶点。机翻

4.The extent of gene amplification may dictate whether MET amplification acts as an oncogenic driver in NSCLC.

因扩增程度可能决定 MET 扩增是否充当 NSCLC 致癌驱动因素。机翻

5.We know that Hepatitis C virus is an oncogenic virus. It's a cancer causing virus and together with HIV may increase the risk of cancers.

我们知道, 丙型肝炎病是一种致癌病。这种癌会引发病并且连带艾滋病一起会增加癌症风险。

6.Targeted treatments for known oncogenic drivers (see Chapter 7) should be given until resistance, before proceeding with chemotherapy with or without immunotherapy.

进行联合或不联合免疫治疗化疗之前，应针对已知致癌驱动因素（参见第 7 章）进行靶向治疗，直至产生耐药性。机翻

7.Likewise, BRAF-mutant tumors have higher RR and longer PFS on ICIs than other oncogenic drivers do, without any clear evidence of differing efficacies between BRAF-mutation subtypes.

同样，与其他致癌驱动因素相比，BRAF 突变肿 ICI 有更高 RR 和更长 PFS，但没有任何明确证据表明 BRAF 突变亚型之间疗效存差异。机翻

8.MET amplification is also a common determinant of AR during treatment with TKIs for other oncogenic drivers such as EGFR, ALK, ROS1, KRAS G12C and NTRK.

使用 TKI 治疗其他致癌驱动因素（例如 EGFR、ALK、ROS1、KRAS G12C 和 NTRK）期间，MET 扩增也是 AR 常见决定因素。机翻

9.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 突变 MET 外显子 14 跳跃突变和 MET 扩增都是 3- -5% NSCLC 患者主要致癌驱动因素； MET 失调 NSCLC 预后较差。机翻

10.However, it should be noted that a negative liquid biopsy result does not rule out an oncogenic driver, and tissue-based testing should be performed if possible.

然而，应该指出是，液体活检结果呈阴性并不能排除致癌驱动因素，如果可能，应进行于组织检测。机翻

11.Although NTRK fusions seem to be mutually exclusive with other oncogenic drivers, these fusions were recently reported in EGFR-mutant NSCLC as a mechanism of AR to EGFR-TKIs.

尽管 NTRK 融合似乎与其他致癌驱动因素相互排斥，但最近 EGFR 突变 NSCLC 中报道了这些融合作为 EGFR-TKI AR 机制。机翻

12.Key points - personalized treatment in advanced NSCLC Approximately 50% of advanced NSCLCs have a known oncogenic alteration, many of which can be managed with targeted therapies.

要点 - 晚期 NSCLC 个性化治疗 大约 50% 晚期 NSCLC 有已知致癌改变，其中许多可以通过靶向治疗来控制。机翻

13.This personalized medicine approach has a large effect on patients' survival, as when a patient with an oncogenic target receives the appropriate targeted therapy the duration of response is longer than previously seen with chemotherapy.

这种个性化医疗方法对患者生存有很大影响，因为当有致癌靶标患者接受适当靶向治疗时，反应持续时间比以前化疗更长。机翻