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Naoko Aragane
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OA 10 - Liquid Biopsy for Genomic Alterations (ID 678)
- Event: WCLC 2017
- Type: Oral
- Track: Advanced NSCLC
- Presentations: 1
- Moderators:Adrian G. Sacher, Pasi A Jänne
- Coordinates: 10/18/2017, 11:00 - 12:30, F201 + F202 (Annex Hall)
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OA 10.08 - Discussant - OA 10.05, OA 10.06, OA 10.07 (ID 10807)
11:00 - 12:30 | Presenting Author(s): Naoko Aragane
- Abstract
- Presentation
Abstract not provided
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P2.03 - Chemotherapy/Targeted Therapy (ID 704)
- Event: WCLC 2017
- Type: Poster Session with Presenters Present
- Track: Chemotherapy/Targeted Therapy
- Presentations: 1
- Moderators:
- Coordinates: 10/17/2017, 09:30 - 16:00, Exhibit Hall (Hall B + C)
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P2.03-009 - Clarification of Mechanisms of Acquired Resistance for Afatinib Using Plasma Samples (ID 7570)
09:30 - 16:00 | Author(s): Naoko Aragane
- Abstract
Background:
It is important to clarification of mechanisms of acquired resistance for epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) to determine the next treatment. EGFR T790M and hepatocyte growth factor (HGF) over expression has been observed in 50 to 60% of lung cancer patients who acquired resistance to the first generation EGFR-TKIs. However mechanisms of acquired resistance for the second generation EGFR-TKI, afatinib have not be clear.
Method:
We analyzed plasma T790M and HGF in twenty lung adenocarcimona patients treated with afatinib. Seven patients treated with afatinib as the first EGFR-TKI treatment and thirteen patients treated as EGFR-TKI re-challenge after acquired resistance for first generation EGFR-TKI. EGFR mutations in plasma DNA were detected using the mutation-biased PCR and quenched probe system. HGF level in plasma was measured by enzyme-linked immunosorbent assay.
Result:
In patients treated with afatinib as the first line treatment, no patients detected plasma T790M before afatinib treatment, but one of seven patients detected plasma T790M at the time of acquired resistance. Five of seven patients detected elevation of plasma HGF level when they had progressive disease. In patients treated with afatinib as EGFR-TKI re-challenge, ten of thirteen patients detected plasma T790M before afatinib treatment and nine of them had also T790M positive at the time of acquired resistance for afatinib. Two of three patients who had not detected plasma T790M before afatinib treatment become plasma T790M positive at the time of acquired resistance. Six patients who detected T790M treated with osimertiib and five of them demonstrated partial response (PR).
Conclusion:
T790M might be also major mechanism of acquired resistance in afatinib. Elevation of plasma HGF level might be detected more high frequency at the time of acquired resistance for afatinib than first generation EGFR-TKIs.
