Prevention and management of lung cancer in China Hong, Qun‐Ying; Wu, Guo-Ming; Qian, Gui‐Sheng ...
Cancer,
September 1, 2015, 2015-Sep-01, 2015-09-00, 20150901, Letnik:
121, Številka:
S17
Journal Article
Ferroptosis is an iron-dependent regulated cell death marked by excessive oxidative phospholipids (PLs). The polyunsaturated fatty acids-containing phospholipids (PUFA-PLs) are highly susceptible to ...lipid peroxidation under oxidative stress. Numerous pulmonary diseases occurrences and degenerative pathologies are driven by ferroptosis. This review discusses the role of ferroptosis in the pathogenesis of pulmonary diseases including asthma, lung injury, lung cancer, fibrotic lung diseases, and pulmonary infection. Additionally, it is proposed that targeting ferroptosis is a potential treatment for pulmonary diseases, particularly drug-resistant lung cancer or antibiotic-resistant pulmonary infection, and reduces treatment-related adverse events.
Long noncoding RNAs (lncRNAs) have been demonstrated to play significant roles in non-small cell lung cancer (NSCLC) progression. Recently, a newly identified lncRNA, LncRNA LINC00668 (LINC00668), ...was reported to be involved in the regulation of progression of several tumors. However, the expression pattern and biological function of LINC00668 in NSCLC remains largely unclear. In this study, we found that LINC00668 expression was significantly up-regulated in both NSCLC tissues and cell lines. we also showed that LINC00668 upregulation was induced by transcription factor STAT3. Clinical investigation demonstrated that high expression level of LINC00668 was associated with advanced TNM stage, histological grade and lymph node metastasis. Moreover, multivariate analysis confirmed LINC00668 expression level to be an independent prognostic indicator for overall survival of NSCLC patients. Functional assays indicated that knockdown of LINC00668 suppressed NSCLC cells proliferation, migration and invasion, and promoted apoptosis. Mechanistic studies indicated that LINC00668 is a direct target of miR-193a, leading to down-regulation in the expression of its target gene KLF7. Our findings suggested that STAT3-induced LINC00668 contributed to NSCLC progression through upregulating KLF7 expression by sponging miR-193a, and may serve as a prognostic biomarker and a potential target for NSCLC.
Medical image segmentation is crucial for accurate diagnosis and treatment in the medical field. In recent years, convolutional neural networks (CNNs) and Transformers have been frequently adopted as ...network architectures in medical image segmentation. The convolution operation is limited in modeling long-range dependencies because it can only extract local information through the limited receptive field. In comparison, Transformers demonstrate excellent capability in modeling long-range dependencies but are less effective in capturing local information. Hence, effectively modeling long-range dependencies while preserving local information is essential for accurate medical image segmentation. In this paper, we propose a four-axis fusion framework called FAFuse, which can exploit the advantages of CNN and Transformer. As the core component of our FAFuse, a Four-Axis Fusion module (FAF) is proposed to efficiently fuse global and local information. FAF combines Four-Axis attention (height, width, main diagonal, and counter diagonal axial attention), a multi-scale convolution, and a residual structure with a depth-separable convolution and a Hadamard product. Furthermore, we also introduce deep supervision to enhance gradient flow and improve overall performance. Our approach achieves state-of-the-art segmentation accuracy on three publicly available medical image segmentation datasets. The code is available at https://github.com/cczu-xiao/FAFuse.
Immunohistochemical staining was positive for cytokeratin (CK) 5/6, CK7, CK8/18, Ki67, P40, P63, carcinoembryonic antigen (CEA), CK19, and sex-determining region Y (SRY)-related high mobility ...group-box 10 protein (SOX-10). Currently, surgery is the preferred treatment, but the tumor mostly occurs in the main airway, thus the traditional surgical approach causes significant trauma and impairs lung function. The tumor has been removed by means of bronchoscopic intervention therapies, such as high-frequency electric knife, argon plasma coagulation, cryotherapy, and laser, to avoid a thoracotomy, reduce trauma, preserve lung tissue, and improve lung function with a low incidence of adverse reactions.
Lung cancer is one of the most common and deadly tumors around the world. Targeted therapy for patients with certain mutations, especially by use of tyrosine kinase inhibitors (TKIs) targeting ...epidermal growth factor receptor (EGFR), has provided significant benefit to patients. However, gradually developed resistance to the therapy becomes a major challenge in clinical practice and an alternative to treat such patients is needed. Herein, we report that apatinib, a novel anti-angiogenic drug, effectively inhibits obtained gefitinib-resistant cancer cells but has no much effect on their parental sensitive cells.
Gefitinib-resistant lung cancer cell line (PC9GR) was established from its parental sensitive line (PC9) with a traditional EGFR mutation after long time exposure to gefitinib. Different concentrations of apatinib were used to treat PC9, PC9GR, and other two lung cancer cell lines for its anti-growth effects. RNA sequencing was performed on PC9, PC9GR, and both after apatinib treatment to detect differentially expressed genes and involved pathways. Protein expression of key cycle regulators p57, p27, CDK2, cyclin E2, and pRb was detected using Western blot. Xenograft mouse model was used to assess the anti-tumor activity of apatinib in vivo.
The established PC9GR cells had over 250-fold increased resistance to gefitinib than its sensitive parental PC9 cells (IC
5.311 ± 0.455 μM vs. 0.020 ± 0.003 μM). The PC9GR resistance cells obtained the well-known T790M mutation. Apatinib demonstrated much stronger ( ~ fivefold) growth inhibition on PC9GR cells than on PC9 and other two lung cancer cell lines, A549 and H460. This inhibition was mostly achieved through cell cycle arrest of PC9GR cells in G1 phase. RNA-seq revealed multiple changed pathways in PC9GR cells compared to the PC9 cells and after apatinib treatment the most changed pathways were cell cycle and DNA replication where most of gene activities were repressed. Consistently, protein expression of p57, CDK2, cyclin E2, and pRb was significantly impacted by apatinib in PC9GR cells. Oral intake of apatinib in mouse model significantly inhibited establishment and growth of PC9GR implanted tumors compared to PC9 established tumors. VEGFR2 phosphorylation in PC9GR tumors after apatinib treatment was significantly reduced along with micro-vessel formation.
Apatinib demonstrated strong anti-proliferation and anti-growth effects on gefitinib resistant lung cancer cells but not its parental sensitive cells. The anti-tumor effect was mostly due to apatinib induced cell cycle arrest and VEGFR signaling pathway inhibition. These data suggested that apatinib may provide a benefit to patients with acquired resistance to EGFR-TKI treatment.
...we used saline flushing and cryobiopsy repeatedly to take out huge blood clots, an intact cast of the bronchial tree, including right lobe, two segmental branches of the upper lobe, and five ...segmental branches of the lower lobe Figure 1B. See PDF The commonly used methods to control massive hemoptysis are iced saline, agents, laser, argon plasma coagulation, bronchial artery embolization, and surgery. 2 Since the patient had massive bleeding in the right-side wall of the lower trachea, conventional treatment was ineffective, and the patient had a collapsed trachea at the same time, Y-style silicone stent was placed through rigid bronchoscopy to compress hemostasis Figure 1C.
Computed tomography images are easy to misjudge because of their complexity, especially images of solitary pulmonary nodules, of which diagnosis as benign or malignant is extremely important in lung ...cancer treatment. Therefore, there is an urgent need for a more effective strategy in lung cancer diagnosis. In our study, we aimed to externally validate and revise the Mayo model, and a new model was established.
A total of 1450 patients from three centers with solitary pulmonary nodules who underwent surgery were included in the study and were divided into training, internal validation, and external validation sets (n = 849, 365, and 236, respectively). External verification and recalibration of the Mayo model and establishment of new logistic regression model were performed on the training set. Overall performance of each model was evaluated using area under receiver operating characteristic curve (AUC). Finally, the model validation was completed on the validation data set.
The AUC of the Mayo model on the training set was 0.653 (95% confidence interval CI: 0.613-0.694). After re-estimation of the coefficients of all covariates included in the original Mayo model, the revised Mayo model achieved an AUC of 0.671 (95% CI: 0.635-0.706). We then developed a new model that achieved a higher AUC of 0.891 (95% CI: 0.865-0.917). It had an AUC of 0.888 (95% CI: 0.842-0.934) on the internal validation set, which was significantly higher than that of the revised Mayo model (AUC: 0.577, 95% CI: 0.509-0.646) and the Mayo model (AUC: 0.609, 95% CI, 0.544-0.675) (P < 0.001). The AUC of the new model was 0.876 (95% CI: 0.831-0.920) on the external verification set, which was higher than the corresponding value of the Mayo model (AUC: 0.705, 95% CI: 0.639-0.772) and revised Mayo model (AUC: 0.706, 95% CI: 0.640-0.772) (P < 0.001). Then the prediction model was presented as a nomogram, which is easier to generalize.
After external verification and recalibration of the Mayo model, the results show that they are not suitable for the prediction of malignant pulmonary nodules in the Chinese population. Therefore, a new model was established by a backward stepwise process. The new model was constructed to rapidly discriminate benign from malignant pulmonary nodules, which could achieve accurate diagnosis of potential patients with lung cancer.
•Tuberculous pleurisy is common, but difficult to diagnose.•Little is known about its proteome in patients.•5101 proteins were quantified, where 903 were differentially expressed between patient and ...control samples.•Protein expression was mostly down, with the minority overly expressed in patient samples.•19 proteins were validated as potential diagnostic markers.
Tuberculous pleurisy is a common type of tuberculosis (TB), but its diagnosis is challenging. This study aimed to profile the protein expression of this disease and identify new diagnostic makers.
Biopsy tissues from patients with tuberculous pleurisy and controls were taken through thoracoscopy, and proteins were extracted for Tandem Mass Tag Mass Spectrometry. Differential protein expression was performed between patients and controls, and the identified proteins were analyzed for pathway enrichment. Selected proteins were further validated in another set of samples using a more quantitative method.
A total of 5101 proteins were detected and quantified in a discovery set of patients and controls. Overall protein expression was quite different between patients and controls. Most proteins were down-expressed, while a minority were overly expressed in the patient samples. At p value < 0.05 and absolute fold change >2, 295 proteins were found to be up-expressed and 608 down-expressed. The top enriched pathways included ECM-receptor interaction, complement and coagulation cascades and focal adhesion. All 19 selected candidates were validated in an independent set of patient and control samples.
This unbiased proteomics approach not only provided unique insights into protein expression and pathways, but also discovered potential diagnostic markers for tuberculous pleurisy.
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