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Han-Min Wang
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P76 - Targeted Therapy - Clinically Focused - EGFR (ID 253)
- Event: WCLC 2020
- Type: Posters
- Track: Targeted Therapy - Clinically Focused
- Presentations: 1
- Moderators:
- Coordinates: 1/28/2021, 00:00 - 00:00, ePoster Hall
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P76.81 - Primary Resistance to EGFR-TKIs in Lung Adenocarcinoma harboring EGFR–RAD51 Fusion: A Brief Report (ID 3497)
00:00 - 00:00 | Presenting Author(s): Han-Min Wang
- Abstract
Introduction
EGFR fusions are rare oncogenic mutations in lung cancer. Growing evidences support the efficacy of targeted therapy in such type of carcinoma. However, we found that some patients did not respond to EGFR tyrosine kinase inhibitors (TKIs).
Methods
Biological samples were sent for next-generation-sequencing(NGS)-based analysis targeting 139 cancer-related genes at the baseline and at disease progression respectively. Tumor response was determined according to RECIST 1.1.
Results
Totally 2 patients harbored de novo EGFR-RAD51 fusion at the Guangdong Lung Cancer Institute from January 1, 2017 to August 1, 2020. Both were diagnosed with metastatic lung adenocarcinoma and had poor progression-free survival to EGFR-TKIs. Patient 1, a 15-year-old female, presented with left chest pain. She was initially treated with erlotinib and progressed with newly lung and bone metastases after 2.1 months. Then she received chemotherapy with carboplatin and pemetrexed, and achieved stable disease after 4 cycles. At disease progression, she refused receiving anti-cancer treatment and died after 1 month. Patient 2, a 33-year-old male, presented with cough and headache. He was treated with first-line osimertinib. Clinical benefit was seen quickly and PS score was improved from 3 to 1 in 1 week. However, initial CT and MRI evaluation performed 4 weeks post-treatment showed newly left pleural effusion while lesions in lung, liver and brain were all shrunk. Then bevacizumab was added to osimertinib for 2 cycles. CT scan revealed liver metastases enlarged though lesions in the lungs and the brain were confirmed as partial response (PR). An extra EGFR amplification appeared in liver metastasis, so osimertinib combined with cetuximab was administered. But he progressed again after 1.3 months. At that moment, brain metastases also progressed dramatically. Mechanisms of resistance were not elucidated. Subsequently, he received the combination of carboplatin, pemetrexed and bevacizumab, resulting in a remarkable response in brain metastases, the liver metastases remained stable and primary lung lesion was still responding. Thus far, he is continuing treatment with chemotherapy and bevacizumab.
Conclusion
We suggested that not all lung adenocarcinoma patients harboring EGFR-RAD51 fusion are sensitive to targeted therapy. The therapeutic conception will need more real-world evidences. Chemotherapy plus bevacizumab might be an option for EGFR-RAD51 fusion-posive patients.
