Lung cancer is the most prevalent cancer and the leading cause of cancer-related deaths worldwide. More than 80% of lung cancer incidences are non-small cell lung cancer (NSCLC), including adenocarcinoma, squamous carcinoma and large-cell lung cancer [1,2]. Although surgical resection is widely applied for patients with all types of NSCLC, different strategies such as radiotherapy and multimodal neoadjuvant chemotherapy are adopted to treat NSCLC. In addition, various mutations or copy number variations such as EGFR, MET, ALK, ROS1 and HER2 have been identified as key drivers of NSCLC, and targeting these mutations by small molecules or monoclonal antibodies significantly improves the prognosis of NSCLC patients. However, there are no targeted medicines for mutations of KRAS at the Gly12 position, which are found in ~30% lung adenocarcinoma. Several genes such as TP53 and LKB1 are commonly co-mutated and render different gene expression profiles that might determine distinct therapeutic strategies [3]. Accordingly, mouse models with the Kras^G12D mutation and simultaneous inactivation of TP53 or LKB1 have been established, which recapture the develop process of human NSCLC and provide platforms to screen and evaluate therapeutic strategies for NSCLC [4].

中文翻译：

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CCL28在Kras突变的非小细胞肺癌小鼠模型中不可或缺的作用。

肺癌是全球最普遍的癌症，也是与癌症相关的死亡的主要原因。超过80％的肺癌发病率是非小细胞肺癌（NSCLC），包括腺癌，鳞状癌和大细胞肺癌[1,2]。尽管外科手术切除术广泛适用于所有类型的NSCLC患者，但仍采用放射疗法和多模式新辅助化疗等不同策略来治疗NSCLC。此外，各种突变或拷贝数变异，例如EGFR，MET，ALK，ROS1和HER2已被确定为NSCLC的关键驱动因素，通过小分子或单克隆抗体靶向这些突变可显着改善NSCLC患者的预后。但是，目前尚无针对Gly12位KRAS突变的靶向药物，这种药物在约30％的肺腺癌中发现。TP53和LKB1等几种基因通常共同突变，并呈现出不同的基因表达谱，可能决定了不同的治疗策略[3]。因此，已经建立了具有Kras ^G12D突变并同时使TP53或LKB1失活的小鼠模型，该模型重获了人类NSCLC的发育过程，并提供了筛选和评估NSCLC治疗策略的平台[4]。