Burden of male hardcore smokers and its characteristics among those eligible for lung cancer screening.
- 作者列表："Park DW","Jang JY","Park TS","Lee H","Moon JY","Kim SH","Kim TH","Yoon HJ","Kang DR","Sohn JW
BACKGROUND:There are few data available about hardcore smokers and their behavioral characteristics among the lung cancer screening (LCS) population. The study investigated the burden of hardcore smokers within the LCS population, and determine the characteristics of hardcore smokers using nationally representative data in South Korea. METHODS:We used data from 2007 to 2012 from the Korean National Health and Nutrition Examination Survey. This study enrolled current male smokers aged 55-74 years. Among them, subjects eligible for LCS were defined as these populations with smoking histories of at least 30 PY. Hardcore smoking was defined as smoking >15 cigarettes per day, with no plan to quit, and having made no attempt to quit. Multivariate logistic regression analyses were used to estimate associations between hardcore smokers and various sociodemographic and other variables. RESULTS:The proportion of hardcore smokers among those who met LCS eligibility criteria decreased from 2007 to 2012 (from 39.07 to 29.47% of the population) but did not change significantly thereafter (P = 0.2770), and that proportion was consistently 10-15% higher than that of hardcore smokers among all male current smokers. The proportion without any plan to quit smoking decreased significantly from 54.35% in 2007 to 38.31% in 2012. However, the smokers who had made no intentional quit attempt in the prior year accounted for more than half of those eligible for LCS, and the proportion of such smokers did not change significantly during the study period (50.83% in 2007 and 51.03% in 2012). Multivariate logistic regression analyses showed that hardcore smokers were older (OR = 1.05, 95% confidence interval [CI] 1.01-1.09) than non-hardcore smokers. Hardcore smokers exhibited higher proportion of depression (OR = 6.55, 95% CI 1.75-24.61) and experienced extreme stress more frequently (OR = 1.93, 95% CI 1.13-3.29). Smokers who did not receive smoking cessation education within the past year were significantly more likely to be hardcore smokers (OR = 4.15, 95% CI 1.30-13.22). CONCLUSIONS:It is important to identify a subset of smokers unwilling or minimally motivated to quit within the context of lung cancer screening. Anti-smoking education should be enhanced to influence hardcore smokers' behavior.
背景: 在肺癌筛查 (LCS) 人群中，关于核心吸烟者及其行为特征的数据很少。该研究调查了LCS人群中铁杆吸烟者的负担，并使用韩国全国代表性数据确定了铁杆吸烟者的特征。 方法: 我们使用了 2007 年至 2012 年韩国国家健康和营养调查的数据。这项研究纳入了 55-74 岁的男性吸烟者。其中，符合LCS条件的受试者被定义为具有至少 30 py的吸烟史的这些人群。核心吸烟被定义为每天吸烟> 15 支，没有戒烟计划，也没有尝试戒烟。使用多变量逻辑回归分析来估计核心吸烟者与各种社会人口统计学和其他变量之间的关联。 结果: 从 2007 年到 2012 年，符合LCS资格标准的人群中，核心吸烟者的比例下降了 (从人口的 39.07 下降到 29.47%) 但此后无明显变化 (p = 0.2770)，在所有男性当前吸烟者中，这一比例始终高于核心吸烟者的 10-15%。没有任何戒烟计划的比例从 2007 年的 54.35% 显著下降到 2012 年的 38.31%。然而，前一年没有有意戒烟的吸烟者占符合LCS条件的一半以上，在研究期间，这种吸烟者的比例没有显著变化 (2007 年为 50.83%，2012 年为 51.03%)。多因素logistic回归分析显示，核心吸烟者比非核心吸烟者年龄大 (or = 1.05，95% 可信区间 [CI] 1.01-1.09)。核心吸烟者表现出较高的抑郁比例 (or = 6.55，95% CI 1.75-24.61)，并且经历极端压力的频率更高 (or = 1.93，95% CI 1.13-3.29)。过去一年内未接受戒烟教育的吸烟者更可能成为核心吸烟者 (or = 4.15，95% CI 1.30-13.22)。 结论: 在肺癌筛查的背景下，确定不愿意或最小动机戒烟的吸烟者子集是很重要的。应加强反吸烟教育，以影响核心吸烟者的行为。
METHODS::Pulmonary artery sling is a rare congenital anomaly of the origin and course of the left pulmonary artery. Patients with this condition typically present with respiratory failure in young infancy, and asymptomatic cases are uncommon. We describe the case of an adult patient with a lung adenocarcinoma of the right upper lobe, extending into the hilum and superior mediastinum, and with a previously unknown pulmonary artery sling anomaly. The local invasiveness of the tumor and the peculiar vascular anatomy contributed to a unique surgical scenario, wherein multiple reconstructive procedures were required.
METHODS::Patients with idiopathic pulmonary fibrosis (IPF) have higher risk of developing lung cancer, for example, squamous cell carcinoma (SCC), and show poor prognosis, while the molecular basis has not been fully investigated. Here we conducted DNA methylome analysis of lung SCC using 20 SCC samples with/without IPF, and noncancerous lung tissue samples from smokers/nonsmokers, using Infinium HumanMethylation 450K array. SCC was clustered into low- and high-methylation epigenotypes by hierarchical clustering analysis. Genes hypermethylated in SCC significantly included genes targeted by polycomb repressive complex in embryonic stem cells, and genes associated with Gene Ontology terms, for example, "transcription" and "cell adhesion," while genes hypermethylated specifically in high-methylation subgroup significantly included genes associated with "negative regulation of growth." Low-methylation subgroup significantly correlated with IPF (78%, vs. 17% in high-methylation subgroup, p = 0.04), and the correlation was validated by additional Infinium analysis of SCC samples (n = 44 in total), and data from The Cancer Genome Atlas (n = 390). The correlation between low-methylation subgroup and IPF was further validated by quantitative methylation analysis of marker genes commonly hypermethylated in SCC (HOXA2, HOXA9 and PCDHGB6), and markers specifically hypermethylated in high-methylation subgroup (DLEC1, CFTR, MT1M, CRIP3 and ALDH7A1) in 77 SCC cases using pyrosequencing (p = 0.003). Furthermore, low-methylation epigenotype significantly correlated with poorer prognosis among all SCC patients, or among patients without IPF. Multivariate analysis showed that low-methylation epigenotype is an independent predictor of poor prognosis. These may suggest that lung SCC could be stratified into molecular subtypes with distinct prognosis, and low-methylation lung SCC that significantly correlates with IPF shows unfavorable outcome.
METHODS::The role of Fyn-related kinase (FRK) in malignant tumors remains controversial. Our study investigated the function of FRK in lung cancer. Immunohistochemistry staining and generating a knockout of FRK by CRISPR/Cas9 in H1299 (FRK-KO-H1299) cells were strategies used to explore the role of FRK. Immunohistochemistry staining indicated that FRK expression was elevated in 223 lung cancer tissues compared to 26 distant normal lung tissues. FRK contributed to poor survival status in lung cancer patients and acted as a predictor for poor prognosis of lung cancer. Knockout of FRK by CRISPR/Cas9 markedly inhibited proliferation, invasion, colony formation and epithelial-mesenchymal transition (EMT) process in the lung cancer cell line H1299. Further exploration indicated that FRK-KO damaged the stemness phenotype of H1299 by inhibiting CD44 and CD133 expression. Seahorse detection and a U-13 C flux assay revealed that FRK-KO induced metabolism reprogramming by inhibiting the Warburg effect and changing the energy type in H1299 cells. Epidermal growth factor stimulation recovered the expression of FRK and biological functions, metabolic reprogramming and stemness phenotype of H1299 cells. FRK plays an oncogenic role in lung cancer cells via a novel regulation mechanism of enhancing the stemness of H1299 cells by inducing metabolism reprogramming, which finally promotes EMT and metastasis. Our study also indicates that FRK could be used as a potential therapeutic target for drug development.