scholarly journals High level of BRD4 promotes non-small cell lung cancer progression

Oncotarget ◽  
2016 ◽  
Vol 7 (8) ◽  
pp. 9491-9500 ◽  
Author(s):  
Yun-Fei Liao ◽  
Yong-Bing Wu ◽  
Xiang Long ◽  
Shu-Qiang Zhu ◽  
Chun Jin ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cancer Progression ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Small Cell Lung ◽  
High Level

scholarly journals Elevation of EIF4G1 promotes non‐small cell lung cancer progression by activating mTOR signalling

2021 ◽  
Vol 25 (6) ◽  
pp. 2994-3005
Author(s):  
Ying Lu ◽  
Shanshan Yu ◽  
Guangxue Wang ◽  
Zuan Ma ◽  
Xuelian Fu ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cancer Progression ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Small Cell Lung ◽  
Mtor Signalling

PD-L1 Gene Polymorphism and High Level of Plasma Soluble Pd-L1 Protein may be aSsociated with Non-Small Cell Lung Cancer

2015 ◽  
Vol 30 (4) ◽  
pp. 364-368 ◽  
Author(s):  
Sensen Cheng ◽  
Jinsong Zheng ◽  
Jingyan Zhu ◽  
Chao Xie ◽  
Xia Zhang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Plasma Levels ◽  
Plasma Concentrations ◽  
Small Cell ◽  
Small Cell Lung ◽  
High Level ◽  
Nsclc Patients ◽  
L1 Protein

Background PD-1 and its ligand PD-L1 belong to the co-inhibition molecules, which can downregulate immune responses. The PD-L1 polymorphism and the level of soluble PD-L1 (sPD-L1) were investigated in non-small cell lung cancer (NSCLC). Methods A total of 288 NSCLC patients and 300 controls were enrolled. An A/C polymorphism at position 8923 in the PD-L1 gene was genotyped using the polymerase chain reaction-restriction fragment length polymorphism method. Results The prevalence of the 8923C allele was significantly higher in NSCLC patients than controls (10.2% versus 5.3%, p = 0.002, odds ratio 2.03, 95% confidence interval 1.30-3.17; data were adjusted for age and sex). NSCLC patients also showed increased plasma levels of sPD-L1 compared to controls (1.92 ng/mL versus 0.91 ng/mL, p<0.001). Furthermore, lung adenocarcinoma patients had higher sPD-L1 levels than patients with squamous cell carcinoma (p<0.01). However, no association was observed between the different genetic variants and plasma concentrations of sPD-L1. Conclusions The PD-L1 8923A/C polymorphism could be associated with increased susceptibility to NSCLC. Plasma levels of sPD-L1 are significantly increased in NSCLC patients, especially those with adenocarcinoma.

scholarly journals Interleukin-35 Expression in Non-Small Cell Lung Cancer is Associated with Tumor Progression

2018 ◽  
Vol 51 (4) ◽  
pp. 1839-1851 ◽  
Author(s):  
Mingfei Sun ◽  
Xianjie Zheng ◽  
Qingjiang Meng ◽  
Yanjun Dong ◽  
Guoyu Zhang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cancer Progression ◽  
Cell Lung Cancer ◽  
Disease Free Survival ◽  
Prognostic Indicator ◽  
Small Cell ◽  
Inflammatory Factor ◽  
Small Cell Lung ◽  
Chemotherapy Drugs

Background/Aims: Lung cancer continues to be the leading cause of cancer related deaths worldwide due to its high incidence, malignant behavior and lack of major advancements in treatment strategy. The occurrence and development of lung cancer is closely related to inflammation. Thus, we conducted the present study to investigate the effects of IL-35 (Interleukin 35), a newly identified anti-inflammatory factor, on non-small cell lung cancer (NSCLC), which accounts for about 85% of all lung cancers. Methods: We first evaluated the IL-35 expression in 384 pairs of NSCLC samples and their adjacent normal mucosa by realtime PCR, ELISA (Enzyme-linked immunoassay) and tissue microarrays. Then the role of IL-35 on patient survival rates, cancer progression and their sensitivity to chemotherapy drugs were assessed. Results: IL-35 was barely expressed in the NSCLC tissues but highly expressed in the adjacent normal tissues. The down-regulation of IL-35 was significantly correlated with the results of American Joint Committee on Cancer stage, differentiation and it was also shown to be an independent prognostic indicator of disease-free survival and overall survival for patients with NSCLC. Overexpression of IL-35 in NSCLC cells suppressed cell migration, invasion, proliferation, colony formation through suppressing β-catenin. IL-35 inhibited NSCLC formation in the mice model and sensitize the cancer cells to chemotherapy drugs. Conclusion: Our results showed that IL-35 plays an inhibitory role in NSCLC development and function as a novel prognostic indicator and a potential therapeutic target.

The overexpression of 14-3-3ζ and Hsp27 promotes non-small cell lung cancer progression

Cancer ◽  
2013 ◽  
Vol 120 (5) ◽  
pp. 652-663 ◽  
Author(s):  
Guang-Yin Zhao ◽  
Jian-Yong Ding ◽  
Jie Gu ◽  
Chun-Lai Lu ◽  
Zong-Wu Lin ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cancer Progression ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Small Cell Lung

scholarly journals Circular RNA circ_0020123 Promotes Non-Small Cell Lung Cancer Progression Through miR-384/TRIM44 Axis

2021 ◽  
Vol Volume 13 ◽  
pp. 75-87
Author(s):  
Qingshan Ma ◽  
Baogang Huai ◽  
Yuting Liu ◽  
Zhongyao Jia ◽  
Qilong Zhao
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cancer Progression ◽  
Cell Lung Cancer ◽  
Circular Rna ◽  
Small Cell ◽  
Small Cell Lung

scholarly journals MET Amplification in Non-Small Cell Lung Cancer (NSCLC)—A Consecutive Evaluation Using Next-Generation Sequencing (NGS) in a Real-World Setting

Cancers ◽  
2021 ◽  
Vol 13 (19) ◽  
pp. 5023
Author(s):  
Christoph Schubart ◽  
Robert Stöhr ◽  
Lars Tögel ◽  
Florian Fuchs ◽  
Horia Sirbu ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Next Generation Sequencing ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Resistance Mechanism ◽  
Small Cell ◽  
Small Cell Lung ◽  
High Level ◽  
Next Generation Sequencing Ngs ◽  
Generation Sequencing

In non-small cell lung cancer (NSCLC), approximately 1–3% of cases harbor an increased gene copy number (GCN) of the MET gene. This alteration can be due to de novo amplification of the MET gene or can represent a secondary resistance mechanism in response to targeted therapies. To date, the gold standard method to evaluate the GCN of MET is fluorescence in situ hybridization (FISH). However, next-generation sequencing (NGS) is becoming more relevant to optimize therapy by revealing the mutational profile of each NSCLC. Using evaluable n = 205 NSCLC cases of a consecutive cohort, this study addressed the question of whether an amplicon based NGS assay can completely replace the FISH method regarding the classification of MET GCN status. Out of the 205 evaluable cases, only n = 9 cases (43.7%) of n = 16 high-level MET amplified cases assessed by FISH were classified as amplified by NGS. Cases harboring a MET GCN > 10 showed the best concordance when comparing FISH versus NGS (80%). This study confirms that an amplicon-based NGS assessment of the MET GCN detects high-level MET amplified cases harboring a MET GCN > 10 but fails to detect the various facets of MET gene amplification in the context of a therapy-induced resistance mechanism.

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