scholarly journals Anti‐PD‐L1/TGF‐βR fusion protein (SHR‐1701) overcomes disrupted lymphocyte recovery‐induced resistance to PD‐1/PD‐L1 inhibitors in lung cancer

2022 ◽  
Author(s):  
Bo Cheng ◽  
Kaikai Ding ◽  
Pengxiang Chen ◽  
Jianxiong Ji ◽  
Tao Luo ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Fusion Protein ◽  
Induced Resistance

scholarly journals Identification of a potent kinase inhibitor targeting EML4-ALK fusion protein in non-small cell lung cancer

MedChemComm ◽  
2017 ◽  
Vol 8 (10) ◽  
pp. 1914-1918
Author(s):  
Lian-Xiang Luo ◽  
Ying Li ◽  
Yu-Zhen Niu ◽  
Yu-Wei Wang ◽  
Qian-Qian Wang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Fusion Protein ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Kinase Inhibitor ◽  
Small Cell ◽  
Small Cell Lung ◽  
Lung Cancers ◽  
Alk Inhibitor

Herein, we reported 5067-0952, a potent ALK inhibitor with pharmacological efficacy in non-small cell lung cancers harboring the ALK fusion oncogene.

Abstract 5530: OTX015, a novel pan BET-BRD inhibitor is active in non-small-cell lung cancer (NSCLC) cell lines bearing the fusion protein EML4-ALK

2014 ◽  
Author(s):  
Ramiro Vázquez ◽  
Lucile Astorgues-Xerri ◽  
Mohamed Bekradda ◽  
Esteban Cvitkovic ◽  
Patrice Herait ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Fusion Protein ◽  
Small Cell Lung Cancer ◽  
Cell Lines ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Nsclc Cell ◽  
Small Cell Lung

AC0010, an Irreversible EGFR Inhibitor Selectively Targeting Mutated EGFR and Overcoming T790M-Induced Resistance in Animal Models and Lung Cancer Patients

2016 ◽  
Vol 15 (11) ◽  
pp. 2586-2597 ◽  
Author(s):  
Xiao Xu ◽  
Long Mao ◽  
Wanhong Xu ◽  
Wei Tang ◽  
Xiaoying Zhang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Animal Models ◽  
Cancer Patients ◽  
Induced Resistance ◽  
Egfr Inhibitor ◽  
Lung Cancer Patients

scholarly journals The SARS-CoV-2 host cell membrane fusion protein TMPRSS2 is a tumor suppressor and its downregulation promotes antitumor immunity and immunotherapy response in lung adenocarcinoma

2021 ◽  
Author(s):  
Zhixian Liu ◽  
Zhilan Zhang ◽  
Qiushi Feng ◽  
Xiaosheng Wang
Keyword(s):  
Lung Cancer ◽  
Cell Membrane ◽  
Fusion Protein ◽  
Membrane Fusion ◽  
Antitumor Immunity ◽  
Host Cell Membrane ◽  
Membrane Fusion Protein ◽  
In Vivo Experiments

Abstract Background Cancer patients are susceptible to SARS-CoV-2 infection. An investigation into the association between the SARS-CoV-2 host cell membrane fusion protein TMPRSS2 and lung cancer is significant, considering that lung cancer is the leading cause of cancer death and that the lungs are the primary organ SARS-CoV-2 attacks. Methods Using five lung adenocarcinoma (LUAD) genomics datasets, we explored associations between TMPRSS2 expression and immune signatures, cancer-associated pathways, tumor progression phenotypes, and clinical prognosis in LUAD by the bioinformatics approach. We validated the findings from the bioinformatics analysis through in vitro and in vivo experiments and clinical samples we collected. Results TMPRSS2 expression levels were negatively correlated with the enrichment levels of both antitumor immune signatures and immunosuppressive signatures in LUAD. However, TMPRSS2 expression levels showed a significant positive correlation with the ratios of immune-stimulatory/immune-inhibitory signatures (CD8 + T cells/PD-L1) in LUAD. TMPRSS2 downregulation correlated with elevated activities of many oncogenic pathways in LUAD, including cell cycle, mismatch repair, p53, and extracellular matrix signaling. TMPRSS2 downregulation correlated with increased proliferation, stemness, genomic instability, tumor advancement, and worse survival in LUAD. In vitro and in vivo experiments validated the association of TMPRSS2 deficiency with increased tumor cell proliferation and invasion and antitumor immunity in LUAD. Moreover, in vivo experiments demonstrated that TMPRSS2-knockdown tumors were more sensitive to BMS-1, an inhibitor of PD-1/PD-L1. Conclusion TMPRSS2 is a tumor suppressor, while its downregulation is a positive biomarker of immunotherapy in LUAD. Our data provide a connection between lung cancer and pneumonia caused by SARS-CoV-2 infection.

Leptomeningeal recurrence after long-term alectinib therapy for non-small cell lung cancer harboring an EML4-ALK fusion protein

2018 ◽  
Vol 37 (1) ◽  
pp. 184-187
Author(s):  
Takahisa Kawamura ◽  
Haruyasu Murakami ◽  
Haruki Kobayashi ◽  
Kazuhisa Nakashima ◽  
Shota Omori ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Fusion Protein ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Small Cell Lung

scholarly journals FL118, a novel camptothecin derivative, is insensitive to ABCG2 expression and shows improved efficacy in comparison with irinotecan in colon and lung cancer models with ABCG2-induced resistance

2015 ◽  
Vol 14 (1) ◽  
Author(s):  
David Westover ◽  
Xiang Ling ◽  
Hong Lam ◽  
Jacob Welch ◽  
Chunyang Jin ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Induced Resistance ◽  
Cancer Models

scholarly journals Identification of mitoxantrone as a new inhibitor of ROS1 fusion protein in non-small cell lung cancer cells

MedChemComm ◽  
2017 ◽  
Vol 8 (3) ◽  
pp. 621-624 ◽  
Author(s):  
Lian-Xiang Luo ◽  
Xing-Xing Fan ◽  
Ying Li ◽  
Xia Peng ◽  
Yin-Chun Ji ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Fusion Protein ◽  
Small Cell Lung Cancer ◽  
Cancer Cells ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Lung Cancer Cells ◽  
Small Cell Lung

scholarly journals Bufalin Reverses HGF-Induced Resistance to EGFR-TKIs in EGFR Mutant Lung Cancer Cells via Blockage of Met/PI3k/Akt Pathway and Induction of Apoptosis

2013 ◽  
Vol 2013 ◽  
pp. 1-9 ◽  
Author(s):  
Xiao-Hong Kang ◽  
Zhen-Ye Xu ◽  
Ya-Bin Gong ◽  
Li-fang Wang ◽  
Zhong-Qi Wang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Growth Factor ◽  
Cancer Cells ◽  
Induced Resistance ◽  
Growth Factor Receptor ◽  
Lung Cancer Cells ◽  
Akt Pathway ◽  
Epidermal Growth ◽  
Egfr Mutant ◽  
Egfr Tkis

The epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs), such as gefitinib and erlotinib, have shown promising therapeutic efficacy in nonsmall cell lung cancer (NSCLC) patients harboring epidermal growth factor receptor- (EGFR-) activating mutation. However, the inevitable recurrence resulting from acquired resistance has limited the clinical improvement in therapy outcomes. Many studies demonstrate that hepatocyte growth factor- (HGF-) Met axis plays an important role in tumor progression and drug sensitivity. HGF may induce resistance to EGFR-TKIs in EGFR mutant lung cancer cells by Met/PI3K/Akt signaling. The purpose of this study was to determine whether bufalin, a major bioactive component of Venenum Bufonis, could reverse HGF-induced resistance to reversible and irreversible EGFR-TKIs in mutant lung cancer cells PC-9, HCC827, and H1975. Our studies showed that bufalin could reverse resistance to reversible and irreversible EGFR-TKIs induced by exogenous HGF in EGFR mutant lung cancer cells by inhibiting the Met/PI3K/Akt pathway and inducing death signaling. These results suggested that bufalin might have a potential to overcome HGF-induced resistance to molecular-targeted drugs for lung cancer.

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