Background: The epidemiological investigation of different cancer types in the global population has reported a decreased risk of bladder cancer (BLCA) in Parkinson’s diseases (PD). SNCA a critical gene in PD pathology have been reported involved in tumorigenesis recently. However, the role of SNCA in BLCA remains unclear. This study aimed to explore the potential value of SNCA as a prognostic diagnostic molecular biomarker in BLCA. Methods: In this study, we explored the expression pattern, prognostic value and promoter methylation level of SNCA in BLCA by GEPIA2, UALCAN, TCGA, GENT2, GEO and c-BioPortal database. Then, we used LinkedOmics database to obtain the co-expression genes of SNCA for further study by WGCNA. We further investigated the correlations between SNCA expression and six main types of immune cell infiltrations and immune signatures by TIMER. Finally, BLCA cell lines treated with 5-Aza-CdR were used to explore the correlation between increased methylation and downregulated mRNA expression. Results: SNCA was downregulated in tumor tissues in TCGA-BLCA, GENT2 and GEO, which was validated in our cohort by qRT-PCR and immunohistochemistry. SNCA was confirmed as an independent predictor of poor overall survival (OS). LinkedOmics analysis suggested that SNCA regulates cell adhesion molecules, cytokine–cytokine receptor interaction, and complement and coagulation cascades. Twenty-two co-expression gene modules were constructed by WGCNA, and most of them were significantly associated with OS and disease-free survival (DFS). Six key genes (CNTN1, DACT3, MYLK1, PDE2A, RBM24, and ST6GALNAC3) screened also significantly correlated with prognosis. There were significant correlations between SNCA expression and immune infiltrations, especially T cell, suggesting that immune infiltration was one of the reasons for the influence of SNCA on prognosis in BLCA. Analysis by ULACAN and c-BioPortal showed that the promoter methylation of SNCA negatively correlated with its mRNA level. Furthermore, BLCA cell treatment with 5-Aza-CdR revealed that SNCA expression levels were upregulated with decreased methylation. Conclusion: Our research showed that SNCA was downregulated in BLCA and negatively correlation with DNA methylation. High SNCA expression was confirmed as an independent risk for prognosis. SNCA probably plays an important role in the infiltration of immune cells, especially with T cells. Thus, SNCA may be a promising prognostic biomarker in BLCA patients.

As the most common histological subtype of primary lung cancer, lung adenocarcinoma (LUAD) causes enormous cancer deaths worldwide. Radiotherapy has been frequently used in LUAD cases, and radiosensitivity is vital for LUAD therapy. This research sought to explore the genetic factors affecting radiosensitivity in LUAD and inner mechanisms. LINC00511, miR-497-5p, and SMAD3 expression in LUAD cells were detected via qRT-PCR and western blot. CCK-8 assays, colony formation, and flow cytometry assays were employed to explore the cell viability, apoptosis, and radiosensitivity in PC-9 and A549 cells. The targeting relationship between LINC00511, miR-497-5p, and SMAD3 was verified by dual luciferase reporter assay. Furthermore, xenograft experiments were performed for the in vivo verification. In conclusion, LINC00511 was overexpressed in LUAD cells, which downregulated downstream miR-497-5p expression and mediately led to SMAD3 activation. LINC00511 downregulation suppressed cell viability while enhanced apoptosis rate in LUAD cells. Also, LINC00511 and SMAD3 were overexpressed, while miR-497-5p was downregulated in LUAD cells exposed to 4Gy irradiation treatment. Moreover, LINC00511 inhibition could block SMAD3 expression and promoted the radiosensitivity both in vitro and in vivo. These findings uncover LINC00511 knockdown promoted miR-497-5p expression and subsequently led to lower SMAD3 level, which enhanced radiosensitivity in LUAD cells. LINC00511/miR-497-5p/SMAD3 axis could be of considerable potential to enhance radiosensitivity in LUAD.

Gastric insufflation for computed tomography (CT)‐guided percutaneous gastrostomy is currently performed via a nasogastric tube or a Chiba needle. However, nasogastric tube placement requires patient pharynx and esophagus, and Chiba needle use is associated with an increased risk of organ damage and prolonged operation time. Herein, we introduce a new method of gastric insufflation via a central venous catheter and explore its safety and efficacy by retrospective analysis of the clinical data of patients who underwent percutaneous gastrostomy using this method in our hospital from April 2021 to March 2022. The extracted data included the following: success rate, operation time, gastric insufflation time, radiation dose, postoperative pain score, and complications. We also compared the preoperative levels of several nutritional indicators (body mass index, hemoglobin, albumin, creatinine, and blood urea nitrogen) with those obtained 1 month postoperatively. A total of 12 patients underwent percutaneous gastrostomy under CT guidance using central venous catheter gastric insufflation. The surgery and gastric insufflation success rates were 100% both. The average operation time, gastric insufflation time, and effective radiation dose were 24.08 ± 5.25 min, 5.08 ± 2.50 min, and 14.16 ± 3.63 mSv, respectively. Based on the World Health Organization scale for pain assessment, five patients reported no postoperative pain and seven patients had mild pain. There were no serious complications, such as stoma infection, peritonitis, gastrointestinal perforation and bleeding, or embedding syndrome. All evaluated nutritional indicators showed improvement at 1 month postoperatively, with statistically significant differences compared to the preoperative values (p < 0.05 for all). In conclusion, CT‐guided percutaneous gastrostomy with central venous catheter gastric insufflation is a safe, effective, and feasible minimally invasive treatment.

Purpose This retrospective study aimed to investigate changes in pulmonary function among patients undergoing computed tomography (CT)-guided microwave ablation (MWA) for the treatment of pulmonary ground-glass nodules following lobectomy. Materials and methods Fifty-two patients with pulmonary ground-glass nodules (GGN) who underwent lobectomy and were subsequently diagnosed with non-small cell lung cancer (NSCLC) were included in the study. Pulmonary function tests (PFTs) were conducted at baseline and again 1 month after microwave ablation (MWA). The assessed parameters included vital capacity (VC), forced vital capacity (FVC), forced expiratory volume in 1 s (FEV1), FEV1 percentage (FEV1%), peak expiratory flow (PEF), maximal voluntary ventilation (MVV), and maximum mid-expiratory flow (MMEF). The measurements obtained 1-month post-MWA were compared to the baseline values. Results The mean values for VC, FVC, FEV1, FEV1%, MMEF, PEF, and MVV at baseline and 1-month post-MWA for all patients were as follows: VC (3.01 ± 0.68vs. 2.88 ± 0.67, P = 0.348), FVC (3.07 ± 0.75 vs. 2.95 ± 0.69, P = 0.430), FEV1 (2.29 ± 0.61 vs. 2.14 ± 0.55, P = 0.228), FEV1% (74.26 ± 7.70 vs. 72.41 ± 9.40, P = 0.316), MMEF (1.88 ± 0.81 vs. 1.74 ± 0.72, P = 0.410), PEF (5.03 ± 1.62 vs. 4.54 ± 1.53, P = 0.179), and MVV (77.69 ± 22.21 vs. 73.15 ± 17.63, P = 0.286). For the eight patients who underwent ablation of two or more lesions simultaneously, the mean values for VC, FVC, FEV1, FEV1%, MMEF, PEF, and MVV at baseline and 1 month post-MWA were as follows: VC (2.67 ± 0.90vs. 3.05 ± 0.97, P = 0.341), FVC (2.82 ± 0.94vs. 3.10 ± 0.92, P = 0.430), FEV1 (1.97 ± 0.69vs. 2.07 ± 0.69, P = 0.709), FEV1% (70.01 ± 7.24 vs. 66.27 ± 4.47, P = 0.082), MMEF (1.28 ± 0.80 vs. 1.35 ± 0.58, P = 0.777), PEF (4.43 ± 1.44 vs. 3.87 ± 1.40, P = 0.074), and MVV (65.22 ± 16.50 vs. 72.26 ± 12.28, P = 0.222). No significant differences were observed in the PFT results before and 1 month after MWA. Conclusions MWA is a localized treatment that spares lung parenchyma. The pulmonary function 1 month after MWA did not statistically differ from baseline levels, suggesting that MWA may not adversely affect pulmonary function.

Ten percent of non-small cell lung cancer patients with epidermal growth factor receptor (EGFR) mutations harbor uncommon variants. These mutations are mainly involved in lung adenocarcinomas but are rare in lung squamous cell carcinoma (LSCC). In 2018, the Food and Drug Administration-approved afatinib for this specific patient population. However, there is limited information regarding the effectiveness of afatinib for LSCC with EGFR mutations. This case report documented a unique case of a patient with LSCC, which had a rare compound EGFR mutation (G719C and S768I) and showed significant response to afatinib treatment, with 10 months of progression-free survival. New NTRK1 and RET gene mutations may play a potential role in the development of acquired resistance to afatinib following clinical progression. This case highlights the importance of genetic profiling in patients with LSCC. Although these patients have a low positive rate of EGFR mutations, searching for EGFR mutations in these patients might broaden their treatment options.

Background: Real-world data on afatinib for patients with non-small cell lung cancer (NSCLC) harboring epidermal growth factor receptor (EGFR) G719X + S768I co-mutations remains limited. This study aims to evaluate the efficacy and safety of afatinib in a relatively large cohort of NSCLC patients with these uncommon mutations in Xuanwei and Fuyuan counties, China. Methods: A retrospective study was conducted on 96 NSCLC patients from Xuanwei and Fuyuan, China, between August 2019 and March 2024. Patients with advanced-stage NSCLC harboring EGFR G719X + S768I co-mutations or single EGFR G719X/S768I mutations who received first-line afatinib treatment were included in the study. The parameters analyzed included the progression-free survival (PFS), and overall survival (OS). While treatment-related adverse events (AEs) were assessed for the safety of afatinib. Results: All of the 96 patients, 59 were female and 37 were male, with a median age was 59.2±9.0 years. The mutations were classified as single EGFR G719X/S768I mutations (n=34; 35.4%) and G719X + S768I co-mutations (n=62; 64.6%). The median progression-free survival (mPFS) for all patients was 12 months (95% CI: 9.5–14.5), and median overall survival (mOS) was 29 months (95% CI: 18.0–40.0). Patients with the G719X + S768I co-mutations exhibited significantly longer mPFS (17 vs. 8 months, P<0.001) and mOS (33 vs. 15 months, P=0.04) compared to those with and single EGFR G719X/S768I mutation. Common treatment-related AEs included diarrhea (n=80; 83.3%), skin rash/acne (n=77; 80.2%), paronychia (n=53; 55.2%), and stomatitis (n=33; 34.4%), all of which were manageable. There was no significant difference in AEs between the two mutation groups. Conclusions: This study represents the largest cohort of NSCLC patients with EGFR G719X + S768I co-mutations treated with first-line afatinib. Our findings confirmed the effectiveness and safety of afatinib in this patient population. Furthermore, the presence of the G719X + S768I co-mutations serves as an independent predictor of favorable PFS for NSCLC patients. This study will provide new clinical evidence supporting afatinib therapy for patients with EGFR G719X + S768I co-mutations, both in China and globally. This study fills an important gap in the existing literature by providing robust, large-scale clinical data, offering new insights for the treatment of NSCLC patients with these uncommon mutations.