Objective This study sought to explore the clinical value of matrix metalloproteinases 12 ( MMP12) in multiple cancers, including lung adenocarcinoma (LUAD). Methods Using >10,000 samples, this retrospective study demonstrated the first pan-cancer analysis of MMP12. The expression of MMP12 between cancer groups and their control groups was analyzed using Wilcoxon rank-sum tests. The clinical significance of MMP12 expression in multiple cancers was assessed using receiver operating characteristic curves, Kaplan–Meier curves, and univariate Cox analysis. A further LUAD-related analysis based on 4565 multi-center and in-house samples was performed to verify the findings regarding MMP12 in pan-cancer analysis partly. Results MMP12 mRNA is highly expressed in 13 cancers compared to their controls, and the MMP12 protein level is elevated in some of these cancers (e.g., colon adenocarcinoma) ( P < .05). MMP12 expression makes it feasible to distinguish 21 cancer tissues from normal tissues (AUC = 0.86). A high MMP12 expression is a prognosis risk factor in eight cancers, such as adrenocortical carcinoma (hazard ratio >1, P < .05). The elevated MMP12 expression is also a prognosis protective factor in breast-invasive carcinoma and colon adenocarcinoma (hazard ratio <1, P < .05). Some pan-cancer findings regarding MMP12 are verified in LUAD—MMP12 expression is upregulated in LUAD at both the mRNA and protein levels ( P < .05), has the potential to distinguish LUAD with considerable accuracy (AUC = .91), and plays a risk prognosis factor for patients with the disease ( P < .05). Conclusions MMP12 is highly expressed in most cancers and may serve as a novel biomarker for the prediction and prognosis of numerous cancers.
Objective To summarize the experience of surgical treatment of pleural empyema in infants. Methods The clinical data of 21 infants with pleural empyema undergone surgical operation in our hospital from January 2005 to August 2010 were retrospectively analyzed. Results All of the infants received surgical operation; 5 patients underwent pulmonary wedge resection, 3 patients underwent lobectomy. Smooth recovery were achieved in all patients; No perioperative death and complication occurred. Conclusion Surgical operation is an effective method for pleural empyema in infants.
Background Clinical signs of dysphagia, pancreatic achalasia, and esophagitis have been reported in patients with COVID-19. However, the causal relationship between COVID-19 and esophageal diseases is not clear. Therefore, we utilized Mendelian randomization to explore the potential association between COVID-19 and esophageal diseases. Methods The summary statistics for a Genome-wide association study (GWAS) were obtained from The COVID-19 Host Genetics Initiative, encompassing four types of COVID-19 as exposure: severe COVID-19, hospitalized COVID-19 versus ambulatory COVID-19, hospitalized COVID-19 versus uninfected, and confirmed COVID-19. Additionally, summary statistics for ten esophageal diseases as outcomes were sourced from the GWAS Catalog and FinnGen databases. Univariate Mendelian randomization (MR) analysis was utilized to thoroughly investigate and validate the potential causal association between COVID-19 and various esophageal conditions, including esophageal varices, Barrett’s esophagus, esophagitis, esophageal obstruction, esophageal ulcer, esophageal perforation, gastroesophageal reflux, congenital esophageal malformations, benign esophageal tumors, and esophageal adenocarcinoma. Results An inverse variance-weighted (IVW) model was utilized for univariate Mendelian randomization (MR) analysis, which revealed that genetic liability in patients with confirmed COVID-19 was associated with esophageal obstruction (OR [95% CI]: 0.5275458 [0.2822400–0.9860563]; p -value = 0.0450699). Furthermore, a suggestive causal association was found between genetic liability and a reduced risk of benign esophageal tumors (OR [95% CI]: 0.2715453 [0.09368493–0.7870724]; p -value = 0.0163510), but with a suggestively increased risk of congenital esophageal malformations (OR [95% CI]: 6.959561 [1.1955828–40.51204]; p -value = 0.03086835). Additionally, genetic liability in hospitalized COVID-19 patients, compared to non-hospitalized COVID-19 patients, was suggestively associated with an increased risk of esophagitis (OR [95% CI]: 1.443859 [1.0890568–1.914252]; p -value = 0.01068201). The reliability of these causal findings is supported by Cochran’s Q statistic and the MR-Egger intercept test. Conclusion The results of this study suggest the existence of a causal relationship between COVID-19 and esophageal diseases, highlighting differing risk effects of COVID-19 on distinct esophageal conditions.
Lung cancer is the most common cancer in the world. The gene expression profiling of lung cancer has been extensively investigated. However, only a few studies have identified the possible pathways and significant genes related to lung cancer. The aim of this study is to explore the large number of lung cancer-related microarray datasets and identify the crucial genes that can benefit the understanding of the progression and development of this disease.To identify the genes that effected lung cancer at the mRNA level, gene set enrichment analysis was used to analyze six selected gene expression datasets.Among the six gene expression datasets, 3 up-regulated and 26 down-regulated pathways were found by gene set enrichment analysis. We found 11 significant genes with P < 0.05 from the results of tight junction meta-analysis of the six data sets.The tight junction pathway plays an important role in the study of the occurrence and development of lung cancer. Significant genes within the pathways will be further discussed in future studies.
Epidermal growth factor receptor (EGFR) is a member of the tyrosine kinase receptor family, which is thought to be involved in the development of cancer, as the EGFR gene is often amplified, and/or mutated in cancer cells. Lung cancer remains one of the most major causes of morbidity and mortality worldwide, accounting for more deaths than any other cancer cause. Gene polymorphism factor has been reported to be an important factor which increases the susceptibility of lung cancer. There lacks a well-documented diagnostic approach for the lung cancer risk, and the etiology of lung cancer is not clear. The current systematic review was performed to explore the association of EGFR gene polymorphism with lung cancer risk. In this review, association of EGFR 181946C > T, 8227G > A gene polymorphism with lung cancer was found, and EGFR Short genotype of cytosine adenine repeat number polymorphism was significantly associated with an increased risk of lung cancer.
Abstract Background Centrosomal protein 55 ( CEP55 ) plays a significant role in specific cancers. However, comprehensive research on CEP55 is lacking in pan-cancer. Methods In-house and multi-center samples ( n = 15,823) were used to analyze CEP55 in 33 cancers. The variance of CEP55 expression levels among tumor and control groups was evaluated by the Wilcoxon rank-sum test and standardized mean difference (SMD). The clinical value of CEP55 in cancers was assessed using receiver operating characteristic (ROC) curves, Cox regression analysis, and Kaplan-Meier curves. The correlations between CEP55 expression and the immune microenvironment were explored using Spearman’s correlation coefficient. Results The data of clustered regularly interspaced short palindromic repeats confirmed that CEP55 was essential for the survival of cancer cells in multiple cancer types. Elevated CEP55 mRNA expression was observed in 20 cancers, including glioblastoma multiforme ( p < 0.05). CEP55 mRNA expression made it feasible to distinguish 21 cancer types between cancer specimens and their control samples (AUC = 0.97), indicating the potential of CEP55 for predicting cancer status. Overexpression of CEP55 was correlated with the prognosis of cancer individuals for 18 cancer types, exhibiting its prognostic value. CEP55 expression was relevant to tumor mutation burden, microsatellite instability, neoantigen counts, and the immune microenvironment in various cancers ( p < 0.05). The expression level and clinical relevance of CEP55 in cancers were verified in lung squamous cell carcinoma using in-house and multi-center samples (SMD = 4.07; AUC > 0.95; p < 0.05). Conclusion CEP55 may be an immune-related predictive and prognostic marker for multiple cancers, including lung squamous cell carcinoma.
Abstract BackgroundEsophageal squamous cell carcinoma (ESCC) ranks the sixth in mortality rates in cancers due to a lack of a specific target of diagnosis and treatment in the early stages. Although Forkhead box M1 (FOXM1) has been reported to be differentially expressed in ESCC, its clinical role and function in ESCC remained unclarified.MethodsData from our hospital and public databases (n = 1906) were combined to estimate how FOXM1 overexpression showed its discriminatory ability between ESCC and non-ESCC esophageal tissues. Downstream targets of FOXM1 were predicted by using Cistrome database. Functional enrichment analyses were performed to explore the potential signaling pathways related to FOXM1 in ESCC. Based on the available clinical parameters, we investigated the prognosis potential of FOXM1 and its targets.ResultsThe pooled standard mean difference (SMD) for FOXM1 is 2.62 (95% CI: 2.08–3.16), indicating that FOXM1 is upregulated in ESCC. FOXM1 has an extremely high discrimination potential in ESCC because the area under the curve (AUC) of the summary receiver operating characteristic curve (sROC) is 0.99 (95% CI: 0.97–0.99). A total of 168 downstream targets were identified, and nine hub genes were screened from them. We found that FOXM1 and its targets were significantly enriched in the cell cycle. Additionally, the correlation between FOXM1 and clinical parameters had not been observed, except for age.ConclusionsFOXM1 is upregulated in ESCC and has an extremely high discrimination potential in ESCC.
Abstract Purpose This study was aimed to identify the risk factors that influence the mortality risk in patients with acute aortic dissection (AAD) within one year after discharge, and aimed to construct a predictive model for assessing mortality risk. Methods The study involved 320 adult patients obtained from the Medical Information Mart for Intensive Care (MIMIC) database. Logistic regression analysis was conducted to identify potential risk factors associated with mortality in AAD patients within one year after discharge and to develop a predictive model. The performance of the predictive model was assessed using the receiver operating characteristic curve (ROC), calibration curve, and decision curve analysis (DCA). To further validate the findings, patient data from the First Affiliated Hospital of Guangxi Medical University (157 patients) were analyzed. Results Univariate and multivariate logistic regression analyses revealed that gender, length of hospital stay, highest blood urea nitrogen (BUN_max), use of adrenaline, and use of amiodarone were significant risk factors for mortality within one year after discharge ( p < 0.05). The constructed model exhibited a consistency index (C-index) and an area under the ROC curve of 0.738. The calibration curve and DCA demonstrated that these indicators had a good degree of agreement and utility. The external validation results of the model also indicated good predictability (AUC = 0.700, p < 0.05). Conclusion The personalized scoring prediction model constructed by gender, length of hospital stays, BUN_max levels, as well as the use of adrenaline and amiodarone, can effectively identify AAD patients with high mortality risk within one year after discharge.
'/%3e%3cuse xlink:href='%23a' transform='rotate(23.036 .093 25.536)'/%3e%3cuse xlink:href='%23a' transform='rotate(45.87 1.273 16.18)'/%3e%3cuse xlink:href='%23a' transform='rotate(69.945 .996 12.078)'/%3e%3cuse xlink:href='%23a' transform='rotate(20.66 -19.689 31.932)'/%3e%3c/svg%3e)