BACKGROUND: Lung cancer ranks as the foremost cause of cancer-related deaths in China, significantly undermining population health and longevity. By analyzing the trends of death and years of life lost caused by lung cancer in Handan from 2017 to 2023, data support is provided for the formulation of prevention and treatment strategies. METHODS: Lung cancer death data in Handan during 2017-2023 were collected. Excel 2010, SPSS 26.0 and Joinpoint 4.9.0.0 were used to analyze the mortality rate of lung cancer, average annual percentage change (AAPC), cause eliminated life expectancy (CELE), potential gains in life expectancy (PGLEs), Fulfillment index, potential years of life lost (PYLL), potential years of life lost rate (PYLLR), and standardized potential years of life lost rate (SPYLLR). RESULTS: The standardized mortality rate of lung cancer in Handan from 2017 to 2023 showed a decreasing trend (AAPC=-7.10%, P<0.01). The CELE of lung cancer increased by 2.49 years (AAPC=0.48%, P<0.05). The life loss rate decreased by 21.43% (AAPC=-4.61%, P<0.05). The Fulfillment index by lung cancer increased with the growth of age from 2017 to 2023. The PYLL, PYLLR, standardized potential years of life lost (SPYLL) and SPYLLR of lung cancer during 2017 to 2023 were 134,219.75 person years, 2.03‰, 98,735.63 person years, and 1.49‰, respectively. The annual PYLLR and SPYLLR showed a decreasing trend (AAPC=-6.34%, -9.34%, respectively, P<0.01). CONCLUSIONS The standardized mortality rate of lung cancer in Handan from 2017 to 2023 showed a decreasing trend, and the impact of lung cancer on life expectancy decreased. The mortality rates of lung cancer showed significant differences among different ages and genders. It is necessary to take good measures to prevent and control lung cancer in males and higher age groups.
Lung Neoplasms/mortality* ; Humans ; Male ; Life Expectancy/trends* ; Female ; China/epidemiology* ; Aged ; Middle Aged ; Aged, 80 and over ; Adult ; Young Adult

Background and objectivehTe CpG island aberrant promoter methylation in the tumor suppressor gene region plays an important role in the process of tumorigenesis. Relevant evidence shows that the promoter methylation of ARS association domain family 1A (ARSSF1A) gene, a tumor suppressor gene, has a close relationship with non-small cell lung cancer (NSCLC) development; therefore, ARSSF1A may be a potential NSCLC biomarker. hTis paper discussed and summa-rized the relationship betweenARSSF1A gene promoter methylation frequency and NSCLC throughmeta-analysis.Methods By searching Medline, EMBASE, CNKI, and Wanfang database, we selected and collected the published articles regarding RASSF1A gene promoter methylation and NSCLC risk according to the marked inclusion and exclusion criteria. Through meta-analysis, combined odds ratio (OR) and 95% confidence interval (CI) data were used to analyze theRASSF1A gene promoter methylation and NSCLC relationship.Results A total of 23 articles were utilized in this study. Results indicated that theARSSF1A gene promoter methylation rate was 41.50% (95%CI: 34%-49%) in NSCLC tissue and was 5.58% (95%CI: 2%-9%) for the control group. Compared with normal lung tissue, ARSSF1A methylation frequency in tumor tissue was sig-niifcantly higher than that of the control group (OR=8.72, 95%CI: 4.88-15.58,P<0.05). Subgroup analysis showed that the ARSSF1A gene promoter methylation rate of tumor tissue was higher than that of plasma group (OR=10.99, 95%CI: 2.48-48.68) and normal control tissue group (OR=8.74, 95%CI: 4.39-17.41).ConclusionhTe rate ofARSSF1A promoter gene methyla-tion in NSCLC patient tissue samples was higher than that of normal lung samples, whereas the rate ofARSSF1A promoter gene methylation in the tissue has more signiifcant effect on lung cancer occurrence. hTis ifnding indicates thatARSSF1A gene promoter methylation could be used as an NSCLC biomarker and was involved in NSCLC carcinogenic effects.

Intracellular nutrients and the rate of energy lfowing in tumor cells are otfen higher than that in normal cells due to the prolonged stress of tumor-speciifc microenvironment. In this context, the metabolism of tumor cells provides the fuel of bio-synthesis and energy required for tumor metastasis. Consistent with this, the abnormal metabolism such as extremely active glucose metabolism and excessive accumulating of fatty acid is also discovered in metastatic tumors. Previous Studies have conifrmed that the regulation of tumor metabolism can affect the tumor metastasis, and some of these have been successfully applied in clinical effective, positive way. hTus, targeting metabolism of tumor cells might be an effectively positive way to prevent the metastasis of tumor. So, our review is focused on the research development of the relationship between tu-mor metabolism and metastasis as well as the underlying mechanism.