scholarly journals Downregulation of death receptor 4 is tightly associated with positive response of EGFR mutant lung cancer to EGFR-targeted therapy and improved prognosis

Theranostics ◽  
2021 ◽  
Vol 11 (8) ◽  
pp. 3964-3980
Author(s):  
Shuo Zhang ◽  
Zhen Chen ◽  
Puyu Shi ◽  
Songqing Fan ◽  
Yong He ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Targeted Therapy ◽  
Positive Response ◽  
Death Receptor ◽  
Egfr Mutant ◽  
Death Receptor 4

scholarly journals Tumor Hypoxia Response After Targeted Therapy in EGFR-Mutant Non-Small Cell Lung Cancer

2015 ◽  
Vol 15 (2) ◽  
pp. 234-242 ◽  
Author(s):  
Nils D. Arvold ◽  
Pedram Heidari ◽  
Anchisa Kunawudhi ◽  
Lecia V. Sequist ◽  
Umar Mahmood
Keyword(s):  
Lung Cancer ◽  
Targeted Therapy ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Tumor Hypoxia ◽  
Small Cell ◽  
Small Cell Lung ◽  
Hypoxia Response ◽  
Egfr Mutant

scholarly journals Understanding Lineage Plasticity as a Path to Targeted Therapy Failure in EGFR-Mutant Non-small Cell Lung Cancer

2020 ◽  
Vol 11 ◽  
Author(s):  
Tatiana Shaurova ◽  
Letian Zhang ◽  
David W. Goodrich ◽  
Pamela A. Hershberger
Keyword(s):  
Lung Cancer ◽  
Targeted Therapy ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Small Cell Lung ◽  
Therapy Failure ◽  
Egfr Mutant

scholarly journals Does neoadjuvant targeted therapy provide an opportunity for resectable EGFR-mutant lung cancer: a real-world retrospective study

2020 ◽  
Vol 12 (10) ◽  
pp. 5324-5335
Author(s):  
Chao Lv ◽  
Yuanyuan Ma ◽  
Qin Feng ◽  
Fangliang Lu ◽  
Yongkun Chi ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Retrospective Study ◽  
Targeted Therapy ◽  
Real World ◽  
Egfr Mutant

scholarly journals Optimizing the Sequence of Anti-EGFR–Targeted Therapy in EGFR-Mutant Lung Cancer

2014 ◽  
Vol 14 (2) ◽  
pp. 542-552 ◽  
Author(s):  
Catherine B. Meador ◽  
Hailing Jin ◽  
Elisa de Stanchina ◽  
Caroline A. Nebhan ◽  
Valentina Pirazzoli ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Targeted Therapy ◽  
Egfr Mutant

The Potential of Death Receptor 4– and 5–Directed Therapies in the Treatment of Lung Cancer

2007 ◽  
Vol 8 (7) ◽  
pp. 413-419 ◽  
Author(s):  
D. Ross Camidge
Keyword(s):  
Lung Cancer ◽  
Death Receptor ◽  
Death Receptor 4

scholarly journals Co-occurring alterations in driver genes impact on EGFR-targeted therapy among patients with EGFR-mutant advanced non–small cell lung cancer

2018 ◽  
Vol 29 ◽  
pp. ix158-ix159
Author(s):  
C. Lu ◽  
J. Kang ◽  
H.-J. Chen ◽  
H.-Y. Tu ◽  
Q. Zhou ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Targeted Therapy ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Small Cell Lung ◽  
Driver Genes ◽  
Egfr Mutant

There is no Significant Association Between Death Receptor 4 (DR4) Gene Polymorphisms and Lung Cancer in Turkish Population

2013 ◽  
Vol 19 (4) ◽  
pp. 779-784 ◽  
Author(s):  
Deniz Taştemir-Korkmaz ◽  
Osman Demirhan ◽  
Sedat Kuleci ◽  
Serap Hastürk
Keyword(s):  
Lung Cancer ◽  
Gene Polymorphisms ◽  
Death Receptor ◽  
Turkish Population ◽  
Death Receptor 4

MET second-site mutations in EGFR-mutant, MET-amplified non-small cell lung cancer after resistance to combinatorial targeted therapy.

2019 ◽  
Vol 37 (15_suppl) ◽  
pp. e20730-e20730
Author(s):  
Jia-Tao Cheng ◽  
Jinji Yang ◽  
Yilong Wu
Keyword(s):  
Lung Cancer ◽  
Targeted Therapy ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Advanced Nsclc ◽  
Genetic Alterations ◽  
Subsequent Treatment ◽  
Small Cell ◽  
Small Cell Lung ◽  
Egfr Mutant

e20730 Background: MET second-site mutations were previously reported in a few cases of MET-amplified or exon 14-mutant advanced non-small-cell lung cancer (NSCLC) treated with MET inhibitors. However, both the frequency of MET second-site mutations and clinical outcome of patients with such genetic alterations have not been investigated, particularly in EGFR-mutant, MET-amplified advanced NSCLC treated with combinatorial targeted therapy. Methods: Retrospectively, from November 2016 to January 2019, 22 patients with EGFR-mutant, MET-amplified advanced NSCLC had sufficient tumor samples after resistance to a combinatorial therapy with both EGFR and MET inhibitors. All tissue samples were detected using Next-generation sequencing (NGS). The progression-free survival (PFS) was calculated the start of subsequent treatment to progressive disease or death from any cause. The overall survival (OS) was calculated from the start of subsequent treatment to death from any cause. Last follow-up was on January 31, 2019. Results: Five kinds of MET second-site mutations were found in 7 patients: D1246N D1228N, D1228H, D1231Y and Y1230H. The frequency of MET second-site mutations was 31.8% (7/22). The median PFS and OS were 3.7 (95%CI: 1.13-6.3) months and 6.9 (95%CI: 0.2-13.7) months respectively. The ORR of EGFR TKIs plus cabozantinib for suchsecond-site mutaant patients was 50% (2/4). However, the ORR of other treatments was 0% (0/3), Two of them received single agent cabozantinib, and PFS was 0.7 and 1.7 months respectively. One had a PFS of 2.5 months with pemetrexed/carboplatin plus bevacizumab. Conclusions: MET second-site mutation might be one of the commonly-seen molecular mechanisms of acquired resistance to combinatorial targeted therapy in EGFR-mutant, MET-amplified advanced NSCLC. Patients with such mutations could respond to cabozantinib plus EGFR TKI. Further more investigations are warranted to improve the efficacy.

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