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Emphysema affects the number and characteristics of solitary pulmonary nodules identified by chest low-dose computed tomography. A study on screenees with high-risk lung cancer recruited in Upper Silesia.


  • 影响因子:1.04
  • DOI:10.20452/pamw.14985
  • 作者列表:"Wachuła E","Szabłowska-Siwik S","Czyżewski D","Kozielski J","Adamek M
  • 发表时间:2020-01-31

INTRODUCTION:Chest low-dose computed tomography (LDCT) has recently been proved effective in lung cancer screening. OBJECTIVES:We aimed to assess the association between the occurrence of emphysema and solitary pulmonary nodules (SPNs) in first‑round screening with LDCT. PATIENTS AND METHODS:A total of 601 asymptomatic volunteers with a smoking history underwent LDCT; 523 patients were assigned to one of the following groups: E, emphysema without nodules (n = 103); E + N, emphysema with coexisting nodules (n = 96); N, nodules without emphysema (n = 142); and NENN, no nodules and no emphysema (n = 182). The effect of emphysema and demographic factors on the profile of SPNs was assessed. RESULTS:Patients in the E + N group were older than those in the N group (median age, 65 vs 63 years; P = 0.001) and they smoked more (median pack‑years, 37.8 vs 32; P = 0.01). Emphysema was detected in 199 of the 523 patients (38%), while nodules, in 238 (45.5%). The number of nodules in the E + N group was 390 (4.1 nodules per patient), and in the N group, 540 (3.8 nodules per patient). Multiple SPNs, of different size and morphology, constituted 93.3% of the nodules in the E + N group. Seven cases of cancer were detected among 238 patients with nodules, and their distribution was similar in the groups with and without emphysema (4.2 per 100 patients in the E + N group and 2.1 per 100 in the N group; P = 0.44). CONCLUSIONS:Emphysema was more frequently associated with multiple SPNs of different morphology among elderly patients with a higher number of smoking pack‑years.


简介: 胸部低剂量计算机断层扫描 (LDCT) 最近在肺癌筛查中被证明是有效的。 目的: 我们的目的是评估肺气肿和孤立性肺结节 (spn) 在LDCT第一轮筛查中的相关性。 患者和方法: 共有 601 名有吸烟史的无症状志愿者接受了LDCT; 523 名患者被分配到以下组之一: E,无结节的肺气肿 (n = 103); E + N,肺气肿伴并存结节 (n = 96); N,结节不伴肺气肿 (n = 142);和NENN,无结节和肺气肿 (n = 182)。评估肺气肿和人口统计学因素对spn的影响。 结果: E + N组的患者年龄大于N组 (中位年龄,65 岁vs 63 岁; P = 0.001),他们吸烟更多 (中位包-年,37.8 vs 32; P = 0.01)。199 例患者中 523 例 (38%) 检测到肺气肿,238 例 (45.5%) 检测到结节。E + N组的结节数目为 390 个 (每例患者 4.1 个结节),N组为 540 个 (每例患者 3.8 个结节).在E + N组中,多个大小和形态不同的spn构成 93.3% 的结节。238 例结节患者中检出 7 例癌,并且它们的分布在有肺气肿和无肺气肿的组中是相似的 (E + N组 4.2/100 患者,N组 2.1/100; P = 0.44)。 结论: 在吸烟人数较多的老年患者中,肺气肿与多种不同形态的spn更频繁相关。



作者列表:["Mammana M","Zuin A","Serra E","Bellini A","Rea F"]

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.

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作者列表:["Hata A","Nakajima T","Matsusaka K","Fukuyo M","Morimoto J","Yamamoto T","Sakairi Y","Rahmutulla B","Ota S","Wada H","Suzuki H","Matsubara H","Yoshino I","Kaneda A"]

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.

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作者列表:["Zhang L","Yang Y","Chai L","Bu H","Yang Y","Huang H","Ran J","Zhu Y","Li L","Chen F","Li W"]

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.

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