Objectives To determine the incidence and intensity of household impoverishment induced by cancer treatment in China. Design Average income and daily consumption per capita of the households and out-of-pocket payments for cancer care were estimated. Household impoverishment was determined by comparing per capita daily consumption against the Chinese poverty line (CPL, US$1.2) and the World Bank poverty line (WBPL, US$1.9) for 2015. Both pre-treatment and post-treatment consumptions were calculated assuming that the households would divert daily consumption money to pay for cancer treatment. Participants Cancer patients diagnosed initially from 1 January 2015 to 31 December 2016 who had received cancer treatment subsequently. Those with multiple cancer diagnoses were excluded. Data sources A household questionnaire survey was conducted on 2534 cancer patients selected from nine hospitals in seven provinces through two-stage cluster/convenience sampling. Findings 5.89% (CPL) to 12.94% (WBPL) households were impoverished after paying for cancer treatment. The adjusted OR (AOR) of post-treatment impoverishment was higher for older patients (AOR=2.666–4.187 for ≥50 years vs <50 years, p<0.001), those resided in central region (AOR=2.619 vs eastern, p<0.01) and those with lower income (AOR=0.024–0.187 in higher income households vs the lowest 20%, p<0.001). The patients without coverage from social health insurance had higher OR (AOR=1.880, p=0.040) of experiencing post-treatment household impoverishment than those enrolled with the insurance for urban employees. Cancer treatment is associated with an increase of 5.79% (CPL) and 12.45% (WBPL) in incidence of household impoverishment. The median annual consumption gap per capita underneath the poverty line accumulated by the impoverished households reached US$128 (CPL) or US$212 (WBPL). US$31 170 395 (CPL) or US$115 238 459 (WBPL) were needed to avoid household impoverishment induced by cancer treatment in China. Conclusions The financial burden of cancer treatment imposes a significant risk of household impoverishment despite wide coverage of social health insurance in China.

Background: Non-small cell lung cancer (NSCLC) accounts for about 85% of lung cancers, and is the leading cause of tumor-related death. Lung adenocarcinoma (LUAD) is the most prevalent subtype of NSCLC. Although significant progress of LUAD treatment has been made under multimodal strategies, the prognosis of advanced LUAD is still poor due to recurrence and metastasis. There is still a lack of reliable markers to evaluate the LUAD prognosis. This study aims to explore novel biomarkers and construct a prognostic model to predict the prognosis of LUAD patients. Methods: The Genomic Data Commons-The Cancer Genome Atlas-Lung Adenocarcinoma (GDC-TCGA-LUAD) dataset was downloaded from the University of California, Santa Cruz (UCSC) Xena browser. The GSE72094 and GSE13213 datasets and corresponding clinical information were downloaded from the Gene Expression Omnibus (GEO) database. By analyzing these datasets using DESeq2 R package and Limma R package, differentially expressed genes (DEGs) were found. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses were used to analyze possible enrichment pathways. A protein-protein interaction (PPI) network was constructed to explore possible relationship among DEGs by using the STRING database. A survival analysis was performed to identify reliable prognostic genes using the Kaplan-Meier method. A multi-omics analysis was performed using the Gene Set Cancer Analysis (GSCA). The Tumor Immune Estimation Score (TIMER) database was used to analyze the association between prognostic genes and immune infiltration. A Spearman correlation analysis was conducted to examine the correlation between prognostic genes and drug sensitivity. A multivariate Cox regression was used to identify independent prognostic factors. Next, a nomogram was constructed using the rms R package. Finally, the expressions of aspartyl-tRNA synthetase 2 (DARS2) and phosphoribosyl aminoimidazole carboxylase (PAICS) were detected using immunohistochemistry (IHC). Results: We screened out 30 DEGs prior to functional enrichment and PPI network analysis revealing potential enrichment pathways and interactions of these DEGs. Then survival analysis revealed the CENPL, DARS2, and PAICS expression was negatively correlated with LUAD prognosis. Additionally, multi-omics analysis showed CENPL, DARS2, and PAICS expressions were significantly higher in LUAD tissues than normal tissues. CENPL, DARS2, and PAICS were all up-regulated in late stage and M1 stage. Correlation analysis indicated CENPL, DARS2, and PAICS may not be associated with activation or suppression of immune cells. Drug sensitivity analysis revealed many potentially effective drugs and small molecule compounds. Moreover, we successfully constructed a robust and stable nomogram by combining the DARS2 and PAICS expression with other clinicopathological variables. Finally, IHC results showed DARS2 and PAICS were significantly up-regulated in LUAD. Conclusions: The CENPL, DARS2, and PAICS expression was negatively correlated with LUAD prognosis. A prognostic model, which integrated DARS2, PAICS, and other clinicopathological variables, was able to effectively predict LUAD patients prognosis.

Liver stiffness, which correlates well with liver fibrosis stage, can be measured noninvasively by transient elastography, also known as Fibroscan. The present study aimed to determine the independent factors influencing Fibroscan detection by multiple regression analysis. A total of 181 patients who required liver biopsy were enrolled. Liver stiffness measurement (LSM) was detected by Fibroscan on the day of liver biopsy, while clinical information and routine biochemical examination results were also collected. Correlation was analyzed by Spearman's correlation, and multiple regression analysis was performed to analyze the independent influencing factors. The results demonstrated that platelet (PLT) levels, serum albumin (ALB), prothrombin activity (PTA) and body mass index (BMI) were independent predictors of liver stiffness. The contribution of these four predictors to the regression equation was in the following descending order: PLT (negative correlation) > ALB (negative correlation) > PTA (negative correlation) > BMI (positive correlation). In conclusion, the parameters of PLT, ALB, PTA and BMI are independent predicting factors affecting Fibroscan detection. Therefore, the diagnosis and evaluation of liver fibrosis should comprehensively consider the results of Fibroscan, and clinical and laboratory examinations.

Purpose: This study is aimed at exploring the role of pyroptosis‐related genes in the development, immune infiltration, and clinical features of lung adenocarcinoma. Method: Pyroptosis‐related genes were searched using online databases, including MSigDB, Gene, and GeneCards. We explored pyroptosis‐related gene expression patterns in lung adenocarcinoma using the UALCAN database. Functional enrichment analysis of pyroptosis‐related genes in lung adenocarcinoma was performed using the Metascape database. A protein–protein interaction network was constructed using the STRING database, and the outcomes were visualized using Cytoscape. The top five core genes were screened utilizing the MCC algorithm with its cytoHubba plugin. The correlation between immune cell infiltration, diagnosis, and prognosis of core genes in lung adenocarcinoma was explored using the TIMER 2.0, TCGA, and Kaplan–Meier plotter databases. A nomogram was constructed to predict the survival of patients with lung adenocarcinoma using Cox regression analysis, and its clinical value was validated. Samples of paraffin‐embedded lung adenocarcinoma tissues were collected and subjected to immunohistochemical tests to verify the expression of core genes in lung adenocarcinoma and adjacent tissues. Results: Overall, 202 genes related to pyroptosis were identified, with 67 upregulated and 60 downregulated in lung adenocarcinomas. The top five core genes—namely, CASP1 (caspase1), PYCARD (PYD and CARD domain‐containing protein), NLRP3 (NOD‐like receptor protein 3), AIM2 (absent in melanoma 2), and NLRP1 (NOD‐like receptor protein 1)—related to lung adenocarcinoma pyroptosis were selected. The correlation analysis of immune cell infiltration showed that CASP1, NLRP3, and AIM2, which showed that pyroptosis was involved in the infiltration of immune cells in the tumor microenvironment and NLRP1 exhibited high diagnostic efficacy, while PYCARD demonstrated poor diagnostic efficacy. High expression of CASP1, NLRP3, and NLRP1 correlated with a better prognosis ( p < 0.05), while elevated AIM2 expression was associated with a poor prognosis ( p < 0.05). However, PYCARD exhibited no significant correlation with prognosis ( p > 0.05). The immunohistochemistry results showed that positive rates of CASP1, NLRP3, AIM2, and NLRP1 were 20%, 15%, 70%, and 10%, respectively, while in adjacent tissues, the positive rates were 60%, 60%, 20%, and70%, indicating high expression of AIM2 and low expression of CASP1, NLRP3, and NLRP1 in lung adenocarcinoma. Conclusion: CASP1, NLRP3, AIM2, and NLRP1 are core pyroptotic genes in lung adenocarcinoma and exhibit a strong correlation with immune cell infiltration, diagnosis, and prognosis of this condition. These genes may be useful in the clinical diagnosis and treatment of patients with lung adenocarcinoma.

Although anaplastic lymphoma kinase tyrosine kinase inhibitors (ALK-TKIs) have improved the survival rates of lung cancer patients with ALK fusion mutations, their effectiveness varies significantly across different subtypes. We report a case of small intestine metastasis in a lung adenocarcinoma patient with co-occurring echinoderm microtubule-associated protein-like 4 (EML4)-ALK fusion variant 3 (V3) and tumor protein 53 (TP53) mutations after distinct responses to ALK-TKIs. A 45-year-old woman was diagnosed with stage IV lung adenocarcinoma with brain metastasis. Next-generation sequencing revealed EML4-ALK V3 and TP53 co-mutations. After the initial treatment with ensartinib, the patient experienced intracranial disease progression. Radiation therapy (RT) was then administered. Despite good response to RT for the intracranial disease, the primary tumor enlarged. Thus, the patient was treated with oral ensartinib concurrent with chemotherapy, with a partial response in both the primary tumor and intracranial metastases. However, after three cycles of treatment, the patient discontinued chemotherapy because of acute kidney injury. Subsequent thoracic RT resulted in a partial response of the primary tumor; however, new brain and bone metastases were detected, prompting a switch to lorlatinib. The patient developed symptoms of intestinal obstruction 14 months after the initial diagnosis. Surgical intervention revealed a poorly differentiated metastatic lung adenocarcinoma of the upper jejunum. Genetic testing confirmed EML4-ALK V3 and TP53 co-mutations and high expression of programmed cell death-ligand 1. Despite pembrolizumab treatment, the patient's condition deteriorated, and she passed away. We reported a rare case of small intestinal metastasis in a lung adenocarcinoma patient with concurrent EML4-ALK V3/TP53 mutations after distinct responses to ALK-TKIs in different lesions. Our findings revealed heterogeneity in ALK mutations and responses to ALK-TKIs, necessitating the close monitoring of genetic subtypes and associated mutations for tailored treatment strategies. Maintaining a heightened awareness of potential intestinal metastasis and vigilance in monitoring intestinal symptoms and abdominal metastases are pivotal for managing advanced lung adenocarcinoma.

Background Brain metastases (BM) from esophageal carcinoma (EC) is clinically rare and has not yet been reported in elderly patients. This study aimed to investigate the clinicopathological characteristics, outcomes and prognostic factors of BM in elderly patients with EC, in order to provide guidance for clinical practice. Methods A total of 20 EC patients older than 65 years who were diagnosed with BM were identified from the fourth Hospital of Hebei Medical University between January 1, 2009 and December 31, 2018. Survival was evaluated by the Kaplan–Meier method and Cox proportional hazards models. Results The median time from diagnosis of EC to BM was 11.8 months (0–249.2 months). The median overall survival (OS) was 4.8 months (1.13–23.3 months), with 20% of patients achieving the 1-year survival rate. Patients with KPS score of ≥70 had a significantly better OS than those with KPS score<70 (8.4 vs. 3.9 months, p = 0.033). Compared to patients without brain radiotherapy, patients with brain radiotherapy showed better outcomes in both median OS (8.4 vs. 2.9 months) and 1-year survival rate (23.1% vs. 14.3%, p = 0.043). The median OS of patients with radiotherapy combined with chemotherapy and/or targeted therapy and radiotherapy alone was 9.7 months (3.4–23.3 months) and 7.2 months (1.7–18.4 months), respectively, with no significant difference between the two groups (p = 0.215). Conclusions Brain radiotherapy provided clinically meaningful survival benefit for elderly patients with BM from EC. Thus, active treatments for those patients might be required.