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Classification of lung nodules based on CT images using squeeze-and-excitation network and aggregated residual transformations.

使用挤压和激发网络和聚集残差变换的基于CT图像的肺结节分类。

  • 影响因子:1.82
  • DOI:10.1007/s11547-019-01130-9
  • 作者列表:"Zhang G","Yang Z","Gong L","Jiang S","Wang L","Zhang H
  • 发表时间:2020-04-01
Abstract

:Lung cancer is pointed as a leading cause of cancer death worldwide. Early lung nodule diagnosis has great significance for treating lung cancer and increasing patient survival. In this paper, we present a novel method to classify the malignant from benign lung nodules based on CT images using squeeze-and-excitation network and aggregated residual transformations (SE-ResNeXt). The state-of-the-art SE-ResNeXt module, which integrates the advantages of SENet for feature recalibration and ResNeXt for feature reuse, has great ability in boosting feature discriminability on imaging pattern recognition. The method is evaluated on the public available LUng Nodule Analysis 2016 (LUNA16) database with 1004 (450 malignant and 554 benign) nodules, achieving an area under the receiver operating characteristic curve (AUC) of 0. 9563 and accuracy of 91.67%. The promising results demonstrate that our method has strong robustness in the classification of nodules. The method has the potential to help radiologists better interpret diagnostic data and differentiate the benign from malignant lung nodules on CT images in clinical practice. To our best knowledge, the effectiveness of SE-ResNeXt on lung nodule classification has not been extensively explored.

摘要

: 肺癌被认为是全世界癌症死亡的主要原因。早期肺结节诊断对肺癌的治疗和提高患者生存率具有重要意义。在本文中,我们提出了一种新的方法,使用挤压和激发网络和聚集残差变换 (SE-ResNeXt),根据CT图像对良性肺结节进行恶性分类。最先进的SE-ResNeXt模块集成了SENet用于特征重新校准和renext用于特征重用的优势,在提高成像模式识别的特征辨别能力方面具有很大的能力。该方法在公共可用的肺结节分析 2016 (LUNA16) 数据库上进行评估,其中有 1004 个 (450 个恶性和 554 个良性) 结节,实现了受试者工作特征曲线下面积 (AUC) 的 0。9563 和 91.67% 的准确率。有前景的结果表明,我们的方法在结节分类中具有很强的鲁棒性。该方法有可能帮助放射科医生更好地解释诊断数据,并在临床实践中区分CT图像上的良性和恶性肺结节。据我们所知,SE-ResNeXt对肺结节分类的有效性尚未得到广泛探索。

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DOI:10.1016/j.athoracsur.2019.04.100
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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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影响因子:6.93
发表时间:2020-01-15
DOI:10.1002/ijc.32532
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.

翻译标题与摘要 下载文献
影响因子:6.93
发表时间:2020-01-01
DOI:10.1002/ijc.32530
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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肺肿瘤方向

肺肿瘤,又叫支气管肺癌,是常见的恶性肿瘤之一。肺肿瘤的治疗为包括手术、中药、放疗、化疗及免疫等多学科的综合治疗。

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