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T. Kinoshita
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P3.02b - Poster Session with Presenters Present (ID 494)
- Event: WCLC 2016
- Type: Poster Presenters Present
- Track: Advanced NSCLC
- Presentations: 1
- Moderators:
- Coordinates: 12/07/2016, 14:30 - 15:45, Hall B (Poster Area)
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P3.02b-026 - Association of EGFR Exon 19 Deletion and EGFR-TKI treatment duration with Frequency of T790M Mutation in EGFR-Mutant Lung Cancer Patients (ID 5143)
14:30 - 14:30 | Author(s): T. Kinoshita
- Abstract
Background:
The most common event responsible for resistance of epidermal growth factor receptor (EGFR)-tyrosine kinase Inhibitor (TKI) is acquisition of the T790M mutation, which occurs in approximately 50% of patients who initially respond to EGFR-TKI. Recently, third-generation EGFR-TKIs have been shown to exert a remarkable effect against T790M resistance mutation-positive non-small cell lung cancer (NSCLC). T790M is an important predictive marker for third-generation EGFR-TKIs; therefore, determining the clinicopathologic characteristics of T790M-harboring NSCLC showing relapse after EGFR-TKI therapy is of high clinical relevance. we evaluated whether T790M mutation is related to clinicopathologic or prognostic factors in patients with relapse of EGFR-mutant NSCLC after treatment with EGFR-TKIs.
Methods:
We retrospectively reviewed T790M status and clinical characteristics of advanced-stage or recurrent NSCLC patients who had received EGFR-TKI treatment and rebiopsy at Kurume University Hospital between March 2005 and December 2015.
Results:
we identified 193 patients with advanced or recurrent EGFR-mutant NSCLC who developed resistance to initial EGFR-TKI treatment. Of these patients, 105 (54%) underwent re-biopsy. Adequate histological specimens were available for 73 of these patients, who were enrolled in the study; 38 (52%) of them had T790M mutation and 35 (48%) did not. T790M mutation was present more frequently in patients with exon 19 deletion mutation (63%, 26 of 41) than in those with L858R mutation (38%, 12 of 32) (p=0.035) and in patients who received EGFR-TKI treatment for at least 10 months in total (71%, 32 of 45) than in those who did not (21%, 6 of 28) (p<0.001). The median PFS after initial EGFR-TKI treatment was longer in the T790M mutation-positive group (13.6 months, 95% CI: 9.2-15.8) than in the negative group (7 months, 95% CI: 3.7-8.5) (p=0.037). The median total duration of EGFR-TKI treatment in patients with T790M mutation was 15.3 months, which was significantly longer than that (8.1 months) in patients without T790M mutation (p<0.001). Multivariate analyze revealed that The type of EGFR mutation (exon 19 deletion mutation versus L858R point mutation, p=0.011, OR=0.21, 95% CI=0.05-0.71) and total duration of EGFR-TKI treatment (>10 months versus <10 months, p<0.001, OR=0.09, 95% CI=0.02-0.28) were significantly associated with the presence of T790M mutation.
Conclusion:
The patients with EGFR exon 19 deletion mutation and long-term treatment with EGFR-TKI exposure demonstrated a high prevalence of T790M mutation. These data are potentially important for clinical decision making in the NSCLC patients with EGFR mutation.
