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Lung adenocarcinoma (LUAD) has become the main histologic type, which account for nearly 40% of lung cancer. The present study aimed to investigate the gene expression signature in smoking related LUAD. A total of 45 smoking related DEGs in LUAD were identified and functional enrichment analysis was also performed. Then Cox's regression model and Kaplan-Meier analysis were used to screen potential prognostic genes. Finally, AURKA and FAM83A were left for further immune-related mechanism exploration. Kaplan-Meier analysis indicated survival rates are related to different immune cell (B cell and Dendritic cell) infiltration levels. Mechanistically, we further explore the correlation between AURKA and FAM83A gene expression levels and tumor-infiltrating lymphocytes (TILs) level as well as their response to immunomodulators. The results suggested that AURKA and FAM83A are highly expressed in smoking related LUAD, and negatively correlated to B cell and Dendritic cell infiltration levels. At the same time, B cell and Dendritic cell infiltration levels also related to the prognosis of LUAD. We further revealed AURKA and FAM83A could be novel targets to improve the prognosis of LUAD through regulated the response to immunomodulators.

BackgroundSurvival prediction for cervical cancer is usually based on its stage at diagnosis or a multivariate nomogram. However, few studies cared whether long-term survival improved after they survived for several years. Meanwhile, traditional survival analysis could not calculate this dynamic outcome. We aimed to assess the improvement of survival over time using conditional survival (CS) analysis and developed a novel conditional survival nomogram (CS-nomogram) to provide individualized and real-time prognostic information.MethodsCervical cancer patients were collected from the Surveillance, Epidemiology, and End Results (SEER) database. The Kaplan–Meier method estimated cancer-specific survival (CSS) and calculated the conditional CSS (C-CSS) at year y+x after giving x years of survival based on the formula C-CSS(y|x) =CSS(y+x)/CSS(x). y indicated the number of years of further survival under the condition that the patient was determined to have survived for x years. The study identified predictors by the least absolute shrinkage and selection operator (LASSO) regression and used multivariate Cox regression to demonstrate these predictors’ effect on CSS and to develop a nomogram. Finally, the CSS possibilities predicted by the nomogram were brought into the C-CSS formula to create the CS-nomogram.ResultsA total of 18,511 patients aged <65 years with cervical cancer from 2004 to 2019 were included in this study. CS analysis revealed that the 15-year CSS increased year by year from the initial 72.6% to 77.8%, 84.5%, 88.8%, 91.5%, 93.5%, 94.8%, 95.7%, 96.4%, 97.3%, 98.0%, 98.5%, 99.1%, and 99.4% (after surviving for 1-13 years, respectively), and found that when survival exceeded 5-6 years, the risk of death from cervical cancer would be less than 5% in 10-15 years. The CS-nomogram constructed using tumor size, lymph node status, distant metastasis status, and histological grade showed strong predictive performance with a concordance index (C-index) of 0.805 and a stable area under the curve (AUC) between 0.795 and 0.816 over 15 years.ConclusionsCS analysis in this study revealed the gradual improvement of CSS over time in long-term survived cervical cancer patients. We applied CS to the nomogram and developed a CS-nomogram successfully predicting individualized and real-time prognosis.

Gamma ray can promote cancer cell apoptosis and cell cycle arrest. It is often used in the clinical treatment of tumors, including lung cancer. In this study, we aimed to explore the role of gamma ray treatment and its correlation with BTG2 in cell proliferation, apoptosis, and cell cycle arrest regulation in a lung cancer cell line. A549 cell viability, apoptosis rate, and cell cycle were investigated after gamma ray treatment. We then used siRNA for BTG2 to detect the effect of BTG2 knockdown on the progress of gamma ray-treated lung cancer cells. Finally, we investigated the signaling pathway by which gamma ray might regulate BTG2. We found that gamma ray inhibited A549 cell viability and promoted apoptosis and cell cycle arrest, while BTG2 knockdown could relieve the effect caused by gamma ray on A549 cells. Moreover, we confirmed that the effect of BTG2 partly depends on p53 expression and gamma ray-promoting BTG2 expression through the JNK/NF-κB signaling pathway. Our study assessed the possible mechanism of gamma ray in tumor treatment and also investigated the role of BTG2 in gamma ray therapy. All these findings might give a deep understanding of the effect of gamma ray on the progression of lung cancer involving BTG2.

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