,Dispensable role of CCL28 in Kras-mutated non-small cell lung cancer mouse models

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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 KrasG12D 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].
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