Migration of a hookwire used as a video-assisted thoracoscopic surgery marker into the splenic artery.
- 作者列表："Torigoe H","Hirano Y","Ando Y","Washio K
:We present a case in which a hookwire that was used as a video-assisted thoracoscopic (VATS) surgery marker migrated into the splenic artery. The patient was a 70-year-old man with an 18-mm ground glass nodule (GGN) in the right S2. As the GGN was not located in the peripheral part of the lung, a percutaneous hookwire was placed as a marker under CT-guided just before the surgery. We performed VATS right S2 segmentectomy to remove the GGN and the marker; however, we could not locate the marker in the specimen. Histopathological examination revealed adenocarcinoma, TisN0M0, stage 0. CT findings after surgery showed that the marker had migrated into the splenic artery. We followed up the patient, and CT examination conducted 1, 3 and 6 months after the surgery showed no further migration and no damage of the splenic artery. We report the complication of percutaneous hookwire migration into a blood vessel.
: 我们介绍了一个病例，其中使用钩针作为视频辅助胸腔镜 (VATS) 手术标记物迁移到脾动脉。患者是一名 70 岁的男性，右侧s2 有 18 毫米磨玻璃结节 (GGN)。由于GGN不位于肺的周围部分，因此在手术前在CT引导下放置经皮钩针作为标记物。我们进行了VATS右侧S2 段切除术以去除GGN和标记物; 然而，我们无法在标本中定位标记物。组织病理学检查示腺癌，TisN0M0，0 期。手术后的CT结果显示标记物已经迁移到脾动脉。我们对患者进行了随访，术后 1 、 3 和 6 个月进行的ct检查显示无进一步迁移，脾动脉无损伤。我们报告经皮钩丝迁移到血管的并发症。
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.