Histological transformation as resistance mechanism of the treatment with EGFR inhibitors in lung adenocarcinoma. Two cases report

2018 ◽  
Author(s):  
Manuela Vazquez Peraita
Keyword(s):  
Lung Adenocarcinoma ◽  
Resistance Mechanism ◽  
Egfr Inhibitors ◽  
Histological Transformation

EGFR Inhibitors in Treatment of Lung Adenocarcinoma

2014 ◽  
Vol 10 (Issue 3-4) ◽  
pp. 47-55
Author(s):  
Ehab Ibrahim
Keyword(s):  
Lung Adenocarcinoma ◽  
Egfr Inhibitors

scholarly journals Squamous cell histological transformation beyond EGFR TKI treatment against EGFR-mutant lung adenocarcinoma

2015 ◽  
Vol 26 ◽  
pp. vii138
Author(s):  
Hayato Koba ◽  
Shingo Nishikawa ◽  
Taro Yoneda ◽  
Takashi Sone ◽  
Hideharu Kimura ◽  
...  
Keyword(s):  
Lung Adenocarcinoma ◽  
Squamous Cell ◽  
Histological Transformation ◽  
Tki Treatment ◽  
Egfr Mutant ◽  
Egfr Tki

scholarly journals Patient-Derived Cells to Guide Targeted Therapy for Advanced Lung Adenocarcinoma

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Seok-Young Kim ◽  
Ji Yeon Lee ◽  
Dong Hwi Kim ◽  
Hyeong -Seok Joo ◽  
Mi Ran Yun ◽  
...  
Keyword(s):  
Lung Adenocarcinoma ◽  
Success Rate ◽  
Targeted Therapies ◽  
Kinase Inhibitor ◽  
Resistance Mechanism ◽  
Patient Treatment ◽  
Driver Mutations ◽  
Preclinical Model ◽  
Egfr Tki

AbstractAdequate preclinical model and model establishment procedure are required to accelerate translational research in lung cancer. We streamlined a protocol for establishing patient-derived cells (PDC) and identified effective targeted therapies and novel resistance mechanisms using PDCs. We generated 23 PDCs from 96 malignant effusions of 77 patients with advanced lung adenocarcinoma. Clinical and experimental factors were reviewed to identify determinants for PDC establishment. PDCs were characterized by driver mutations and in vitro sensitivity to targeted therapies. Seven PDCs were analyzed by whole-exome sequencing. PDCs were established at a success rate of 24.0%. Utilizing cytological diagnosis and tumor colony formation can improve the success rate upto 48.8%. In vitro response to a tyrosine kinase inhibitor (TKI) in PDC reflected patient treatment response and contributed to identifying effective therapies. Combination of dabrafenib and trametinib was potent against a rare BRAF K601E mutation. Afatinib was the most potent EGFR-TKI against uncommon EGFR mutations including L861Q, G719C/S768I, and D770_N771insG. Aurora kinase A (AURKA) was identified as a novel resistance mechanism to olmutinib, a mutant-selective, third-generation EGFR-TKI, and inhibition of AURKA overcame the resistance. We presented an efficient protocol for establishing PDCs. PDCs empowered precision medicine with promising translational values.

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