Objective: Amongst the current detections of tumor markers, measurement of serum tumor markers is the most convenient and the safest way. However, there are few promising serum tumor markers with confirmed prognostic value in NSCLC (non-small-cell lu

Background: The aim of this study was to determine the demographic profile of driver gene alterations, especially low‐frequency gene alterations in Chinese patients with non‐small cell lung cancer (NSCLC).Methods: A total of 7395 Chinese patients with NSCLC were enrolled in the study. Next‐generation sequencing (NGS) was performed on formalin‐fixed paraffin‐embedded specimens collected via either surgical resection or biopsy.Results: The frequent genomic alterations found in the study were EGFR mutations (51.7%), KRAS mutations (13.1%), MET alterations (5.6%; 3.2% copy number gains and 0.5% exon 14 skipping mutation), HER2 alterations (7.0%; 2.0% copy number gains and 5.4% mutations), ALK alterations (7.2%; 3.9% rearrangements), RET rearrangements (1.4%), ROS1 rearrangements (0.9%), and NTRK rearrangements (0.6%). The EGFR mutation rate was found to be significantly higher in women than in men (69.1% vs. 38.5%, P < 0.001), while the KRAS mutation (17.5% vs. 7.3%, P < 0.001) and MET alteration rates (6.5% vs. 4.5%, P < 0.001) were significantly higher in men than in women. The EGFR mutation rate tended to decrease with age in the group aged >40 years, while the KRAS mutation rate tended to increase with age. The HER2 mutation (13.9% vs. 6.7%, P < 0.001) and ALK alteration rates (14.3% vs. 6.9%, P < 0.001) were significantly higher in the group aged <40 years than in groups aged 40 years or older.Conclusions: The frequency of different driver genes was diverse in different age‐gender groups, and the results of this study may assist clinicians in clinical decision‐making and the development of public healthcare strategies in the future.Key points: Significant findings of the study: This study demonstrated that the frequency of different driver genes was diverse in different age‐gender groups. What this study adds It may enable clinicians to make clinical decisions, and assist government, pharmaceutical researchers and insurance companies develop public healthcare strategies.

Background: Sphingolipids not only serve as structural components for maintaining cell membrane fluidity but also function as bioactive molecules involved in cell signaling and the regulation of various biological processes. Their pivotal role in cancer cell development, encompassing cancer cell proliferation, migration, angiogenesis, and metastasis, has been a focal point for decades. However, the contribution of sphingolipids to the complexity of tumor microenvironment promoting cancer progression has been rarely investigated.Methods: Through the integration of publicly available bulk RNA‐seq and single‐cell RNA‐seq data, we conducted a comprehensive analysis to compare the transcriptomic features between tumors and adjacent normal tissues, thus elucidating the intricacies of the tumor microenvironment (TME).Results: Disparities in sphingolipid metabolism (SLM)‐associated genes were observed between normal and cancerous tissues, with the TME characterized by the enrichment of sphingolipid signaling in macrophages. Cellular interaction analysis revealed robust communication between macrophages and cancer cells exhibiting low SLM, identifying the crucial ligand‐receptor pair, macrophage inhibitory factor (MIF)‐CD74. Pseudo‐time analysis unveiled the involvement of SLM in modulating macrophage polarization towards either M1 or M2 phenotypes. Categorizing macrophages into six subclusters based on gene expression patterns and function, the SPP1+ cluster, RGS1+ cluster, and CXCL10+ cluster were likely implicated in sphingolipid‐induced M2 macrophage polarization. Additionally, the CXCL10+, AGER+, and FABP4+ clusters were likely to be involved in angiogenesis through their interaction with endothelial cells.Conclusion: Based on multiple scRNA‐seq datasets, we propose that a MIF‐targeted strategy could potentially impede the polarization from M1 to M2 and impair tumor angiogenesis in low‐SLM non‐small cell lung cancer (NSCLC), demonstrating its potent antitumor efficacy.

Esophageal cancer is one of the most commonly diagnosed malignant tumors, especially in north China. Surgery is one of the major treatments. However, for locally advanced cases, surgery alone does not achieve an ideal prognosis. As a result of rapid development in recent years, neoadjuvant chemotherapy, neoadjuvant radiotherapy or neoadjuvant chemoradiotherapy followed by surgery are becoming the “standard treatment pattern” for patients with locally advanced esophageal cancer, and an improvement in prognosis is evident. With the gradual application of immunotherapy in esophageal cancer, neoadjuvant immunotherapy has also shown an important role. This article mainly focuses on the history and current status of neoadjuvant treatment and its future role in the treatment of esophageal cancer.