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Computed tomography-guided microcoil placement for localizing small pulmonary nodules before uniportal video-assisted thoracoscopic resection.


  • 影响因子:1.82
  • DOI:10.1007/s11547-019-01077-x
  • 作者列表:"Refai M","Andolfi M","Barbisan F","Roncon A","Guiducci GM","Xiumè F","Salati M","Tiberi M","Giovagnoni A","Paci E
  • 发表时间:2020-01-01

PURPOSE:The increasing number of computed tomography (CT) performed allows the more frequent identification of small, solid pulmonary nodules or ground-glass opacities. Video-assisted thoracic surgery (VATS) represents the standard in most lung resections. However, since VATS limit is the digital palpation of the lung parenchyma, many techniques of nodule localization were developed. The aim of this study was to determine the feasibility and safety of CT-guided microcoil insertion followed by uniportal VATS wedge resection (WR). MATERIALS AND METHODS:Retrospective study in a single institution, including patients undergone CT-guided microcoil insertion prior to uniportal VATS resection between May 2015 and December 2018. The lesion was identified using fluoroscopy. RESULTS:Forty-six consecutive patients were enrolled (22 male and 24 female). On CT: 5 cases of GGO, 2 cases of semisolid nodules, 39 cases of solid nodules. The median pathologic tumor size was 1.21 cm. Neither conversion to thoracotomy nor microcoil dislodgement was recorded. All patients underwent uniportal VATS WR (9/46 underwent completion lobectomy after frozen section). WR median time was 105 min (range 50-150 min). No patients required intraoperative re-resection for positive margins. After radiological procedure, 1 case of hematoma and 2 cases of pneumothorax were recorded. Four complications occurred in the postoperative period. The mean duration of chest drain and length of stay were 2.9 and 4.6 days, respectively. CONCLUSIONS:CT-guided microcoil insertion followed by uniportal VATS resection was a safe and feasible procedure having a minimal associated complications rate and offering surgeons the ease of localization of small intrapulmonary nodules.


目的: 越来越多的计算机断层扫描 (CT) 可以更频繁地识别小的实性肺结节或磨玻璃影。电视胸腔镜手术 (VATS) 代表了大多数肺切除术的标准。然而,由于VATS限制是肺实质的数字触诊,因此开发了许多结节定位技术。本研究的目的是确定CT引导下微弹簧圈插入后单孔VATS楔形切除术 (WR) 的可行性和安全性。 材料和方法: 在单一机构中进行回顾性研究,包括 2015 年 5 月至 2018 年 12 月期间在单操作胸腔镜手术切除前接受CT引导下微弹簧圈插入的患者。通过透视检查确定病变。 结果: 共入组 46 例患者 (男 22 例,女 24 例)。CT: GGO 5 例,半固态结节 2 例,实性结节 39 例。肿瘤中位病理大小为 1.21厘米cm,无中转开胸及微弹簧圈脱落。所有患者均接受单孔VATS WR (9/46 在冷冻切片后接受完整肺叶切除术)。WR中位时间为 105 min (范围 50-150 min)。没有患者需要术中再次切除阳性切缘。术后记录血肿 1 例,气胸 2 例。术后出现 4 例并发症。胸腔引流的平均持续时间和住院时间分别为 2.9 天和 4.6 天。 结论: CT引导下微弹簧圈插入后单操作孔VATS切除是一种安全可行的手术,其相关并发症发生率最低,并为外科医生提供了肺内小结节的定位便利。



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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