Good Response to Gefitinib in Lung Adenocarcinoma of Complex Epidermal Growth Factor Receptor ( EGFR ) Mutations with the Classical Mutation Pattern

2008 ◽  
Vol 13 (12) ◽  
pp. 1276-1284 ◽  
Author(s):  
Shang‐Gin Wu ◽  
Yih‐Leong Chang ◽  
Ya‐Chieh Hsu ◽  
Jenn‐Yu Wu ◽  
Chih‐Hsin Yang ◽  
...  
Keyword(s):  
Epidermal Growth Factor Receptor ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Lung Adenocarcinoma ◽  
Growth Factor Receptor ◽  
Egfr Mutations ◽  
Mutation Pattern ◽  
Epidermal Growth ◽  
Classical Mutation

scholarly journals B7-H3-Induced Signaling in Lung Adenocarcinoma Cell Lines with Divergent Epidermal Growth Factor Receptor Mutation Patterns

2020 ◽  
Vol 2020 ◽  
pp. 1-8
Author(s):  
Meng Ding ◽  
Haixiu Liao ◽  
Nannan Zhou ◽  
Ying Yang ◽  
Shihe Guan ◽  
...  
Keyword(s):  
Epidermal Growth Factor Receptor ◽  
Targeted Therapy ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Lung Adenocarcinoma ◽  
Cell Lines ◽  
Growth Factor Receptor ◽  
Egfr Mutations ◽  
Adenocarcinoma Cell ◽  
Epidermal Growth

The cosignal molecule B7-H3 is gaining attention due to its abnormal expression and abundant signal transduction in many types of malignancies. B7-H3-induced signaling includes at least three cascades: PI3K/AKT, JAK2/STAT3, and Raf/MEK/ERK1/2, which are also involved in epidermal growth factor receptor- (EGFR-) triggered signaling in lung adenocarcinoma cells. However, the correlation between B7-H3-induced signaling and EGFR signaling, and between B7-H3-targeted immunotherapy and EGFR-targeted therapy in lung adenocarcinoma, remains to be elucidated. Herein we find that knockout of B7-H3 gene decreased cell survival and increased EGFR-tyrosine kinase inhibitor gefitinib susceptibility of both H3255 and HCC827 cells, two lung adenocarcinoma cell lines harboring EGFR L858R (exon 21) and Del E746-A750 (exon 19) mutations, respectively. B7-H3 deletion resulted in dramatic reduction of phosphorylation level of AKT and STAT3 in H3255 cells while having mild-to-moderate suppression on AKT, STAT3, and ERK1/2 in HCC827 cells. Gefitinib had similar effects with B7-H3 deletion both in H3255 and HCC827 cells. Furthermore, B7-H3 ablation had significant synergistic effects with gefitinib in HCC827 cells. Collectively, our study reveals B7-H3-induced signaling in lung adenocarcinoma cell lines with divergent EGFR mutations, and a translational potential of combined targeted therapy of B7-H3 and EGFR in lung adenocarcinoma with EGFR Del E746-A750 mutation.

Induction gefitinib followed by concurrent chemoradiotherapy in patients with unresectable stage IIIA/b lung adenocarcinoma harboring mutations of epidermal growth factor receptor: Three case reports.

2012 ◽  
Vol 30 (15_suppl) ◽  
pp. e17510-e17510
Author(s):  
Yoshitsugu Horio ◽  
Chiaki Kondo ◽  
Jangchul Park ◽  
Junichi Shimizu ◽  
Kimihide Yoshida ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Epidermal Growth Factor Receptor ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Lung Adenocarcinoma ◽  
Concurrent Chemoradiotherapy ◽  
Locally Advanced ◽  
Growth Factor Receptor ◽  
Egfr Mutations ◽  
Epidermal Growth

e17510 Background: Gefitinib has shown good activity in lung cancer harboring mutations in the epidermal growth factor receptor (EGFR) gene. However, how to integrate gefitinib into concurrent chemoradiotherapy for unresectable locally advanced non-small cell lung cancer (NSCLC) with EGFR mutations is uncertain. Methods: We present three cases of locally advanced lung adenocarcinoma with EGFR mutation, which were treated with gefitinib followed by weekly paclitaxel and carboplatin concurrent with radiation. Three female patients (median age, 73 years; range, 61–77 years) received induction gefitinib 150 mg daily for 1-2 months followed by weekly paclitaxel 40 mg/m2 weekly over 1 hour; carboplatin at AUC (area under the curve) of 2 weekly over 1 hour; and radiation therapy of 60 Gy in 30 fractions. Results: Gefitinib induced very rapid response within the first month without pulmonary toxicity. Subsequent concurrent chemoradiotherapy was performed with safety. One patient recurred as hematogenous lung metastases at 5 months after treatment. The remaining two patients are well doing without adverse events. Conclusions: The very quick response to induction gefitinib and sequential chemoradiotherapy may be an effective treatment with good tolerance. We believe that this treatment strategy deserves further evaluation in unresectable locally advanced NSCLC with EGFR mutations.

scholarly journals EPIDERMAL GROWTH FACTOR RECEPTOR (EGFR) AND CARCINOEMBRYONIC ANTIGEN (CEA) RELATIONSHIP OF LUNG ADENOKARSINOMA IN SAIFUL ANWAR HOSPITA MALANG

2017 ◽  
Vol 13 (2) ◽  
pp. 173
Author(s):  
Normawati Normawati ◽  
Suryanti Dwi Pratiwi ◽  
Nanik Setijowati
Keyword(s):  
Epidermal Growth Factor Receptor ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Lung Adenocarcinoma ◽  
Carcinoembryonic Antigen ◽  
Egfr Mutation ◽  
Growth Factor Receptor ◽  
Egfr Mutations ◽  
Serum Cea ◽  
Epidermal Growth

Abstract: EGFR mutations is associated with sensitivity to tyrosine kinase inhibitors (TKI’s) therapy which are found in Lung Adenocarcinoma. There are some limitations in detecting EGFR mutation. CEA is also expected to predict treatment efficiency of EGFR-TKI's therapy. In this study, we investigated the relationship between serum Carcinoembryonic antigen (CEA) and Epidermal Growth Factor Receptor (EGFR) Mutations in Lung Adenocarcinoma patient. Methods : The research was conducted in Dr. Saiful Anwar General Hospital Malang. From May 2014 to November 2015, 54 lung adenocarcinoma patients who had underwent measurements of EGFR  mutation and serum CEA level were retrospectively recruited. None of them had surgery, radiotherapy, chemotherapy and  targeted therapy. EGFR mutation was detected using PCR, serum CEA levels were analyzed using electrochemical luminescence. Result: Abnormal serum levels of CEA were significantly associated with EGFR mutation (95% CI, P=0,043) with an odds ratio of 3.4 (95% CI: 1.010-11.451). The area under the ROC curve for CEA was 0.558 (95% CI, P=0.078). Conclusion: Serum CEA is associated with mutation of EGFR in lung adenocarcinoma patients.  Keywords : Lung cancer, adenocarcinoma, EGFR, CEA

Good response to pemetrexed in patients of lung adenocarcinoma with epidermal growth factor receptor (EGFR) mutations

Lung Cancer ◽  
2011 ◽  
Vol 72 (3) ◽  
pp. 333-339 ◽  
Author(s):  
Shang-Gin Wu ◽  
Chih-Hsin Yang ◽  
Chong-Jen Yu ◽  
Jih-Hsiang Lee ◽  
Ya-Chieh Hsu ◽  
...  
Keyword(s):  
Epidermal Growth Factor Receptor ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Lung Adenocarcinoma ◽  
Growth Factor Receptor ◽  
Egfr Mutations ◽  
Epidermal Growth

Phase III Study of Afatinib or Cisplatin Plus Pemetrexed in Patients With Metastatic Lung Adenocarcinoma With EGFR Mutations

2013 ◽  
Vol 31 (27) ◽  
pp. 3327-3334 ◽  
Author(s):  
Lecia V. Sequist ◽  
James Chih-Hsin Yang ◽  
Nobuyuki Yamamoto ◽  
Kenneth O'Byrne ◽  
Vera Hirsh ◽  
...  
Keyword(s):  
Epidermal Growth Factor Receptor ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Lung Adenocarcinoma ◽  
Growth Factor Receptor ◽  
Phase Iii ◽  
Egfr Mutations ◽  
Phase Iii Study ◽  
Epidermal Growth ◽  
Exon 19

Purpose The LUX-Lung 3 study investigated the efficacy of chemotherapy compared with afatinib, a selective, orally bioavailable ErbB family blocker that irreversibly blocks signaling from epidermal growth factor receptor (EGFR/ErbB1), human epidermal growth factor receptor 2 (HER2/ErbB2), and ErbB4 and has wide-spectrum preclinical activity against EGFR mutations. A phase II study of afatinib in EGFR mutation–positive lung adenocarcinoma demonstrated high response rates and progression-free survival (PFS). Patients and Methods In this phase III study, eligible patients with stage IIIB/IV lung adenocarcinoma were screened for EGFR mutations. Mutation-positive patients were stratified by mutation type (exon 19 deletion, L858R, or other) and race (Asian or non-Asian) before two-to-one random assignment to 40 mg afatinib per day or up to six cycles of cisplatin plus pemetrexed chemotherapy at standard doses every 21 days. The primary end point was PFS by independent review. Secondary end points included tumor response, overall survival, adverse events, and patient-reported outcomes (PROs). Results A total of 1,269 patients were screened, and 345 were randomly assigned to treatment. Median PFS was 11.1 months for afatinib and 6.9 months for chemotherapy (hazard ratio [HR], 0.58; 95% CI, 0.43 to 0.78; P = .001). Median PFS among those with exon 19 deletions and L858R EGFR mutations (n = 308) was 13.6 months for afatinib and 6.9 months for chemotherapy (HR, 0.47; 95% CI, 0.34 to 0.65; P = .001). The most common treatment-related adverse events were diarrhea, rash/acne, and stomatitis for afatinib and nausea, fatigue, and decreased appetite for chemotherapy. PROs favored afatinib, with better control of cough, dyspnea, and pain. Conclusion Afatinib is associated with prolongation of PFS when compared with standard doublet chemotherapy in patients with advanced lung adenocarcinoma and EGFR mutations.

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