PurposeThis study used the Surveillance, Epidemiology, and End Results (SEER) data to investigate the changes in incidence, treatment, and survival of lung cancer from 1973 to 2015.Patients and methodsThe clinical and epidemiological data of patients with lung cancer were obtained from the SEER database. Joinpoint regression models were used to estimate the rate changes in lung cancer related to incidence, treatment, and survival.ResultsFrom 1973 to 2015, the average incidence of lung cancer was 59.0/100,000 person-years. The incidence increased initially, reached a peak in 1992, and then gradually decreased. A higher incidence rate was observed in males than in females and in black patients than in other racial groups. Since 1985, adenocarcinoma became the most prevalent histopathological type. The surgical rate for lung cancer was about 25%, and treatment with chemotherapy showed an increasing trend, while the radiotherapy rate was in downward trend. The surgical rate for non-small-cell lung cancer (NSCLC) was higher than that for small cell lung cancer (SCLC), while chemotherapy for SCLC far exceeded that for NSCLC. Treatment with chemotherapy and radiotherapy for advanced stage had higher rate than early stage. The 5-year relative survival rate of lung cancer increased with time, but <21%.ConclusionIn the past four decades, the lung cancer incidence increased initially and then gradually decreased. Surgical rate experienced a fluctuant reduction, while the chemotherapy rate was in upward trend. The 5-year relative survival rate increased with years, but was still low.

Abstract:The air quality in China, particularly the PM 2.5 (particles less than 2.5 μm in aerodynamic diameter) level, has become an increasing public concern because of its relation to health risks. The distribution of PM 2.5 concentrations has a close relationship with multiple geographic and socioeconomic factors, but the lack of reliable data has been the main obstacle to studying this topic. Based on the newly published Annual Average PM 2.5 gridded data, together with land use data, gridded population data and Gross Domestic Product (GDP) data, this paper explored the spatial-temporal characteristics of PM 2.5 concentrations and the factors impacting those concentrations in China for the years of 2001-2010. The contributions of urban areas, high population and economic development to PM 2.5 concentrations were analyzed using the Geographically Weighted OPEN ACCESS Int. J. Environ. Res. Public Health 2014, 11 174Regression (GWR) model. The results indicated that the spatial pattern of PM 2.5 concentrations in China remained stable during the period 2001-2010; high concentrations of PM 2.5 are mostly found in regions with high populations and rapid urban expansion, including the Beijing-Tianjin-Hebei region in North China, East China (including the Shandong, Anhui and Jiangsu provinces) and Henan province. Increasing populations, local economic growth and urban expansion are the three main driving forces impacting PM 2.5 concentrations.

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Background: Esophageal squamous cell carcinoma (ESCC) is among the most prevalent causes of cancerrelated death in adults. Tumor microenvironment (TME) has been associated with therapeutic failure and lethal outcomes for patients. However, published reports on the heterogeneity and TME in ESCC are scanty. Methods: Five tumor samples and five corresponding non-malignant samples were subjected to scRNA-seq analysis. Bulk RNA sequencing data were retrieved in publicly available databases. Findings: From the scRNA-seq data, a total of 128,688 cells were enrolled for subsequent analyses. Gene expression and CNV status exhibited high heterogeneity of tumor cells. We further identified a list of tumorspecific genes and four malignant signatures, which are potential new markers for ESCC. Metabolic analysis revealed that energy supply-related pathways are pivotal in cancer metabolic reprogramming. Moreover, significant differences were found in stromal and immune cells between the esophagus normal and tumor tissues, which promoted carcinogenesis at both cellular and molecular levels in ESCC. Immune checkpoints, regarded as potential targets for immunotherapy in ESCC were significantly highly expressed in ESCC, including LAG3 and HAVCR2. Eventually, we constructed a cell-to-cell communication atlas based on cancer cells and immune cells and performed the flow cytometry, qRT-PCR, immunofluorescence, and immunohistochemistry analyses to validate the results. Interpretation: This study demonstrates a widespread reprogramming across multiple cellular elements within the TME in ESCC, particularly in transcriptional states, cellular functions, and cell-to-cell interactions. The findings offer an insight into the exploration of TME and heterogeneity in the ESCC and provide new therapeutic targets for its clinical management in the future.