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Search results for: NSCLC

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#33080551   2020/08/23 To Up

Association of baseline peripheral-blood eosinophil count with immune checkpoint inhibitor-related pneumonitis and clinical outcomes in patients with non-small cell lung cancer receiving immune checkpoint inhibitors.

Immune checkpoint inhibitors (ICIs) have revolutionized the oncologic treatment landscape, but have been accompanied by immune-related adverse events (irAEs). ICI-related pneumonitis (ICI-pneumonitis) is a potentially fatal irAE. However, the risk factors associated with ICI-pneumonitis remain unclear. There is an urgent need to identify risk factors for ICI-pneumonitis using reliable and accessible parameters. Here, we aimed to identify baseline peripheral-blood biomarkers correlated with ICI-pneumonitis and clinical outcomes in patients with advanced non-small cell lung cancer (NSCLC) who were treated with ICIs.
Xiangling Chu, Jing Zhao, Juan Zhou, Fei Zhou, Tao Jiang, Sen Jiang, Xiwen Sun, Xiaofang You, Fengying Fengying, Shengxiang Ren, Caicun Zhou, Chunxia Su

2502 related Products with: Association of baseline peripheral-blood eosinophil count with immune checkpoint inhibitor-related pneumonitis and clinical outcomes in patients with non-small cell lung cancer receiving immune checkpoint inhibitors.



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#33079622   2020/10/20 To Up

Metastatic sites as predictors in advanced NSCLC treated with PD-1 inhibitors: a systematic review and meta-analysis.

Programmed cell death protein 1 (PD-1) inhibitors are the first-line treatment for advanced non-small-cell lung cancer (NSCLC) patients. However, their efficacy in metastatic NSCLC patients remains controversial.
Yangyun Huang, Lihuan Zhu, Tianxing Guo, Wenshu Chen, Zhenlong Zhang, Wujin Li, Xiaojie Pan

1050 related Products with: Metastatic sites as predictors in advanced NSCLC treated with PD-1 inhibitors: a systematic review and meta-analysis.

1600400Tests100ug100ul100ug Lyophilized100ug Lyophilized100ug100 assays100ug Lyophilized1000 assays

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#33079008   2020/10/20 To Up

Frequency and types of mutations in Moroccan patients with non-small cell lung cancer.

Mutations in the epidermal growth factor receptor () gene are commonly observed in non-small cell lung cancer (NSCLC), particularly in adenocarcinoma histology. The frequency of mutations is ethnicity-dependent, with a higher proportion reported in Asian populations than Caucasian populations. There is a lack of data on these mutations in north Africa.
Mohamed Lemine Sow, Hind El Yacoubi, Badreddine Moukafih, Salif Balde, Gloria Akimana, Salma Najem, Siham El Khoyaali, Halima Abahssain, Aicha Chaibi, Shah Zeb Khan, Dario Trapani, Asmae Benzekri, Merieme Ghaouti, Lamia Gamra, Amina Mestari, Fouad Kettani, Younes Rahali, Hind Mrabti, Ibrahim Elghissassi, Hassan Errihani

1351 related Products with: Frequency and types of mutations in Moroccan patients with non-small cell lung cancer.



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#33079003   2020/10/20 To Up

Prognostic impact of serum procalcitonin in non-small cell lung cancer.

Increased serum procalcitonin (PCT), a well-known biomarker for sepsis, has been reported in several cancer types. We aimed to investigate the prognostic impact of PCT in non-small cell lung cancer (NSCLC).
Shigehisa Kajikawa, Wataru Ohashi, Yasutaka Kato, Masaya Fukami, Toshiyuki Yonezawa, Mika Sato, Kenshi Kosaka, Toshio Kato, Hiroyuki Tanaka, Satoru Ito, Etsuro Yamaguchi, Akihito Kubo

1475 related Products with: Prognostic impact of serum procalcitonin in non-small cell lung cancer.



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#33078899   2020/10/20 To Up

Revealing the subtyping of non-small cell lung cancer based on genomic evolutionary patterns by multi-region sequencing.

Accurately classifying patients with non-small cell lung cancer (NSCLC) from the perspective of tumor evolution has not been systematically studied to date. Here, we reconstructed phylogenetic relationships of somatic mutations in 100 early NSCLC patients (327 lesions) through reanalyzing the TRACERx data. Based on the genomic evolutionary patterns presented on the phylogenetic trees, we grouped NSCLC patients into three evolutionary subtypes. The phylogenetic trees among three subtypes exhibited distinct branching structures, with one subtype representing branched evolution and another reflecting the early accumulation of genomic variation. However, in the evolutionary pattern of the third subtype, some mutations experienced selective sweeps and were gradually replaced by multiple newly formed subclonal populations. The subtype patients with poor prognosis had higher intra-tumor heterogeneity and subclonal diversity. We combined genomic heterogeneity with clinical phenotypes analysis and found that subclonal expansion results in the progression and deterioration of the tumor. The molecular mechanisms of subtype-specific Early Driver Feature (EDF) genes differed across the evolutionary subtypes, reflecting the characteristics of the subtype itself. In summary, our study provided new insights on the stratification of NSCLC patients based on genomic evolution that can be valuable for us to understand the development of pulmonary tumor profoundly.
Gaoming Liao, Xin Liang, Yanyan Ping, Yong Zhang, Jianlong Liao, Yihan Wang, Xiaobo Hou, Zedong Jiang, Xiaoqiu Dong, Chaohan Xu, Yun Xiao

2316 related Products with: Revealing the subtyping of non-small cell lung cancer based on genomic evolutionary patterns by multi-region sequencing.

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#33078895   2020/10/20 To Up

Organophosphate-pesticides induced survival mechanisms and APE1-mediated Nrf2 regulation in non-small-cell lung cancer cells.

Epidemiological and molecular studies have indicated that environmental exposure to organophosphate pesticides (OPPs) is associated with increased cancer risk; however, the underlying molecular mechanisms still need to be explained. Increasing cancer incidence is linked to OPPs-induced oxidative stress (OS). Our study evaluates monocrotophos (MCP) and chlorpyrifos (CP)-induced OS responses and apurinic/apyrimidinic endonuclease 1 (APE1) role in human non-small-cell lung cancer (NSCLC) cells. Our prior study has implicated OPPs-induced base excision repair (BER)-pathway dysregulation and APE1-mediated regulation of transcription factor (TF) c-jun in A549 cells. We further investigated the effects of MCP and CP on apoptosis, proliferation, and APE1's redox-regulation of nuclear factor-like 2 (Nrf2). Data demonstrates that MCP and CP at subtoxic concentrations induced reactive oxygen species generation and oxidative DNA base damage 8-oxo-dG lesions in NCI-H1299 cells. CP moderately upregulated the apoptosis-inducing factor (AIF) in A549 cells, however, it did not trigger other pro-apoptotic factors viz. caspase-9 and caspase-3, suggesting early caspase-independent apoptosis. However, dose-dependent AIF-downregulation was observed for MCP treatment. Furthermore, CP and MCP treatments upregulated proliferating cell nuclear antigen levels. Immunofluorescent confocal imaging showed the colocalization of APE1 with Nrf2 in 10 µM CP- and MCP-treated NCI-H1299 cells. Immunoprecipitation confirmed that APE1 and Nrf2 physically interacted, indicating the role of APE1-mediated Nrf2 activation following OPPs treatment. This study suggests that low concentration MCP and CP exposure generates OS along with DNA damage, and modulates apoptosis, and APE1-mediated Nrf2 activation, which might be considered as the possible mechanism promoting lung cancer cell survival, suggesting that APE1 may have the potential to become a therapeutic target for the treatment of NSCLC.
Shweta Thakur, Bibekananda Sarkar, Monisha Dhiman, Anil K Mantha

2006 related Products with: Organophosphate-pesticides induced survival mechanisms and APE1-mediated Nrf2 regulation in non-small-cell lung cancer cells.

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#33078819   2020/10/20 To Up

Dietary flavone from the vine triggers human lung adenocarcinoma apoptosis autophagy.

Among all types of cancers, lung cancer ranks first in morbidity and mortality, and non-small cell lung cancer (NSCLC) accounts for 80-85% of all lung cancer cases. Chemotherapy has shown promising results, but the accompanying side-effects cannot be neglected. Herein, we introduce novel flavones (TVF), which were characterized as 3-caffeoylquinic acid, 5-caffeoylquinic acid, quercetin-3-O-rutinoside, and kaempferol-3-O-rutinoside by UPLC-MS/MS, derived from the vine of Tetrastigma hemsleyanum (TV), a traditional Chinese herb and food. TVF exhibited outstanding anti-cancer abilities at the in vitro and in vivo level, and markedly triggered apoptosis via the Bax/Bcl-2/caspase-9/caspase-3 pathway. The intrinsic mechanism study illustrated that TVF might induce apoptosis by activating autophagy by inhibiting the Akt-mTOR pathway, and the main component of TVF, quercetin-3-O-rutinoside, enabled THR308 site binding to block the phosphorylation of Akt, which was further evidenced by molecular docking computation. Our study reveals the excellent anti-cancer ability and inner mechanism of TVF, suggesting TVF as a potential candidate for clinical drug exploitation or dietary supplementation in cancer medication and prevention, providing a promising strategy for cancer chemotherapy.
Yonglu Li, Xinyu Feng, Yiru Zhang, Yaxuan Wang, Xin Yu, Ruoyi Jia, Ting Yu, Xiaodong Zheng, Qiang Chu

1988 related Products with: Dietary flavone from the vine triggers human lung adenocarcinoma apoptosis autophagy.

100ug Lyophilized 100ul24 Membranes/Box 100 UG4 Arrays/Slide 100ul100 ug

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#33078531   2020/10/20 To Up

Tumor invasion in the central airway is a risk factor for early-onset checkpoint inhibitor pneumonitis in patients with non-small cell lung cancer.

Anti-programmed death-1 (PD-1) immunotherapy can cause immune-related pneumonitis, also known as checkpoint inhibitor pneumonitis (CIP). CIP that develops early after the initiation of anti-PD-1 immunotherapy is important because it is more severe than CIP that develops later. However, only a few studies have examined the risk factors for early-onset CIP. Previous studies have reported several risk factors for CIP, including imaging findings of airway obstruction adjacent to lung tumors. However, the utility of this factor is debatable. Therefore, we investigated potential risk factors for early-onset CIP, including tumor invasion in the central airway (TICA), in patients with non-small cell lung cancer (NSCLC) receiving anti-PD-1 therapy.
Mitsuhiro Moda, Haruhiro Saito, Terufumi Kato, Ryo Usui, Tetsuro Kondo, Yoshiro Nakahara, Shuji Murakami, Kouji Yamamoto, Kouzo Yamada

1663 related Products with: Tumor invasion in the central airway is a risk factor for early-onset checkpoint inhibitor pneumonitis in patients with non-small cell lung cancer.

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#33078469   2020/10/19 To Up

ZNF300 promotes chemoresistance and aggressive behaviour in non-small-cell lung cancer.

Chemoresistance induced by cisplatin has become the major impediment to lung cancer chemotherapy. This study explored the potential chemoresistant genes and underlying mechanisms of chemoresistance in NSCLC.
Shilong Yu, Zhi Ao, Yi Wu, Liyuan Song, Peng Zhang, Xiaokang Li, Min Liu, Pin Qian, Ruijie Zhang, Xihua Li, Yan Chen, Xuanbin Wang, Xianhui Wang, Xuzhi Ruan, Guisheng Qian, Fuyun Ji

2510 related Products with: ZNF300 promotes chemoresistance and aggressive behaviour in non-small-cell lung cancer.



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#33078208   2020/10/19 To Up

E2F1-mediated repression of WNT5A expression promotes brain metastasis dependent on the ERK1/2 pathway in EGFR-mutant non-small cell lung cancer.

Brain metastasis (BM) is associated with poor prognosis in patients with advanced non-small cell lung cancer (NSCLC). Epidermal growth factor receptor (EGFR) mutation reportedly enhances the development of BM. However, the exact mechanism of how EGFR-mutant NSCLC contributes to BM remains unknown. Herein, we found the protein WNT5A, was significantly downregulated in BM tissues and EGFR-mutant samples. In addition, the overexpression of WNT5A inhibited the growth, migration, and invasion of EGFR-mutant cells in vitro and retarded tumor growth and metastasis in vivo compared with the EGFR wide-type cells. We demonstrated a molecular mechanism whereby WNT5A be negatively regulated by transcription factor E2F1, and ERK1/2 inhibitor (U0126) suppressed E2F1's regulation of WNT5A expression in EGFR-mutant cells. Furthermore, WNT5A inhibited β-catenin activity and the transcriptional levels of its downstream genes in cancer progression. Our research revealed the role of WNT5A in NSCLC BM with EGFR mutation, and proved that E2F1-mediated repression of WNT5A was dependent on the ERK1/2 pathway, supporting the notion that targeting the ERK1/2-E2F1-WNT5A pathway could be an effective strategy for treating BM in EGFR-mutant NSCLC.
Huanhuan Li, Fan Tong, Rui Meng, Ling Peng, Jiaojiao Wang, Ruiguang Zhang, Xiaorong Dong

2743 related Products with: E2F1-mediated repression of WNT5A expression promotes brain metastasis dependent on the ERK1/2 pathway in EGFR-mutant non-small cell lung cancer.



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