There are so called oncogenic or tumor producing genes.

有所谓的致癌或产生肿瘤的基。

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

大约 50% 的晚期 NSCLC 具有已知的致癌改变（图 7.1）。

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，是多种儿童实体瘤的新兴治疗靶点。

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

基扩增的程度可能决定 MET 扩增是否充当 NSCLC 的致癌驱动。

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的风险。

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

在进行联合或不联合免疫治疗的化疗之前，应针对已知的致癌驱动（见第 7 章）进行靶向治疗，直至产生耐药性。

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，与其他致癌驱动相比，BRAF 突变肿瘤在 ICI 上具有更高的 RR 更长的 PFS，但没有任何明确证据表明 BRAF 突变亚型之间的疗效存在差异。

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.

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

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 MET 扩增都是 3- -5% NSCLC 患者的主要致癌驱动； MET 失调的 NSCLC 预后较差。

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，应该指出的是，液体活检结果呈阴性并不能排除致癌驱动，如果可能，应进行基于组织的检测。

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相互排斥，但最近在 EGFR 突变 NSCLC 中报道了这些融合作为 EGFR-TKI 的 AR 机制。

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 的个性化治疗 大约 50% 的晚期 NSCLC 具有已知的致癌改变，其中许多可以通过靶向治疗来控制。

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的生存有很大影响，为当具有致癌靶标的患者接受适当的靶向治疗时，反应持续时间比以前的化疗更长。