Quantitative membrane proteomics applying narrow range peptide isoelectric focusing for studies of small cell lung cancer resistance mechanisms

PROTEOMICS ◽  
2008 ◽  
Vol 8 (15) ◽  
pp. 3008-3018 ◽  
Author(s):  
Hanna Eriksson ◽  
Johan Lengqvist ◽  
Joel Hedlund ◽  
Kristina Uhlén ◽  
Lukas M. Orre ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Isoelectric Focusing ◽  
Cell Lung Cancer ◽  
Narrow Range ◽  
Resistance Mechanisms ◽  
Small Cell ◽  
Cancer Resistance ◽  
Small Cell Lung ◽  
Membrane Proteomics

scholarly journals Extensive Disease Small Cell Lung Cancer Dose-Response Relationships: Implications for Resistance Mechanisms

2010 ◽  
Vol 5 (11) ◽  
pp. 1826-1834 ◽  
Author(s):  
David J. Stewart ◽  
Constance Johnson ◽  
Adriana Lopez ◽  
Bonnie Glisson ◽  
Jay M. Rhee ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Dose Response ◽  
Resistance Mechanisms ◽  
Small Cell ◽  
Small Cell Lung ◽  
Extensive Disease

scholarly journals RNA Aptamer-targeted Inhibition of NF-κB Suppresses Non-small Cell Lung Cancer Resistance to Doxorubicin

2008 ◽  
Vol 16 (1) ◽  
pp. 66-73 ◽  
Author(s):  
Jing Mi ◽  
Xiuwu Zhang ◽  
Zahid N Rabbani ◽  
Yingmiao Liu ◽  
Srinevas K Reddy ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Rna Aptamer ◽  
Cancer Resistance ◽  
Small Cell Lung ◽  
Targeted Inhibition ◽  
Resistance To Doxorubicin

Resistance mechanisms to osimertinib in EGFR-mutated advanced non-small-cell lung cancer: A multicentric retrospective French study

Lung Cancer ◽  
2019 ◽  
Vol 137 ◽  
pp. 149-156 ◽  
Author(s):  
Camille Mehlman ◽  
Jacques Cadranel ◽  
Gaelle Rousseau-Bussac ◽  
Roger Lacave ◽  
Anaïs Pujals ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Resistance Mechanisms ◽  
Small Cell ◽  
Small Cell Lung ◽  
French Study ◽  
Egfr Mutated

scholarly journals Chemotherapy Immunophenoprofiles in Non‐Small‐Cell Lung Cancer by Personalized Membrane Proteomics

2020 ◽  
Vol 14 (2) ◽  
pp. 1970064
Author(s):  
Denise Utami Putri ◽  
Po‐Hao Feng ◽  
Yuu‐Hueih Hsu ◽  
Kang‐Yun Lee ◽  
Feng‐Wen Jiang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Small Cell Lung ◽  
Membrane Proteomics

Clinical outcomes of various resistance mechanisms of osimertinib in Chinese advanced non-small cell lung cancer patients.

2019 ◽  
Vol 37 (15_suppl) ◽  
pp. e20530-e20530
Author(s):  
Puyuan Xing ◽  
Li Junling ◽  
Xuezhi Hao ◽  
Yuxin Mu ◽  
Shouzheng Wang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Clinical Outcomes ◽  
Cell Lung Cancer ◽  
Progression Free Survival ◽  
Resistance Mechanisms ◽  
Small Cell ◽  
Egfr Mutations ◽  
Small Cell Lung ◽  
Kras Mutations

e20530 Background: Increasing efforts have been invested in elucidating the resistance mechanisms to osimertinib. Major resistance mechanisms include but not limited to acquired EGFR mutations, predominantly C797, mutations in bypass pathways and small cell lung cancer (SCLC) transformation. However, no study has comprehensively investigated clinical outcomes of various mechanisms of resistance. Methods: 103 T790M positive advanced Chinese non-small cell lung cancer (NSCLC) patients who progressed on 1st generation EGFR-TKI were enrolled. Targeted sequencing, using a panel consisting of 168 lung cancer related genes, was performed on paired plasma samples collected prior to osimertinib and after the development of disease progression (PD) to profile mutation spectrum. 7 patients with no mutation detected at PD were excluded from analyses. Results: Major acquired mutations included 25% EGFR mutations, predominantly C797 and L792, 16% MET amplification, 8% TP53 mutations, 4% KRAS mutations, 4% RET fusions, 4% ERBB2 amplification and 6.25% RB1 mutations. Acquired RB1 mutation may indicate the possibility of SCLC transformation. Approximately, 30% of patients with no known resistance mechanisms at PD. In this cohort, we had 61 patients with 19 deletion and 35 patients with EGFR L858R prior to the initiation of osimertinib. We revealed patients with 19del acquired more mutations ( p= 0.014) and were more likely to acquire mutations in MAP/PI3Kpathway ( p= 0.04) and TP53 at PD ( p= 0.021). On the other hand, acquired ERBB2 amplifications were only detected in L858R-mutant patients ( p= 0.047). Furthermore, 36 patients preserved T790M and 60 patients lost T790M at PD. Our data revealed patients retaining T790M, often associated with activation of bypass signaling pathways or continued EGFR activation through tertiary mutations, had a longer progression-free survival (PFS) ( p= 0.047) and overall survival (OS) ( p= 0.04) comparing to patients with T790M loss, often with diverse and EGFR-independent mechanisms. We also show that patients with acquired C797S had significantly longer PFS ( p= 0.031), while patients with acquired MET amplifications had significantly shorter PFS ( p= 0.033). Conclusions: Collectively, we revealed differential clinical outcomes associated with various resistance mechanisms, representing an important step in advancing the understanding of resistance mechanisms of osimertinib.

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