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I. De Aguirre
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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-014 - Monitoring of T790M Mutation in Serum for Prediction of Response to Third Generation Inhibitors (ID 4097)
14:30 - 14:30 | Author(s): I. De Aguirre
- Abstract
Background:
The emergence of T790M mutation (T790M) represents the main mechanism of acquired resistance (AR) to 1[st] and 2[nd] generation tyrosine kinase inhibitors (TKIs) in EGFR mutant patients (p). Recently, 3[rd] generation inhibitors (T790Mi) have demonstrated activity in EGFR mutant (mu) patients with AR to TKIs harboring T790M. Serum and plasma have been used as an alternative to tissue to detect both sensitizing EGFRmu and T790M. We evaluated if (1) T790M could be monitored along T790Mi therapy in p with baseline T790M in serum, (2) T790M loss could be correlated to clinical and radiographic response, and (3) T790M disappears soon in rapid responders.
Methods:
10 p out of a total of 15 T790M+p treated with T790Mi were selected according the baseline T790M+ in serum. Baseline characteristics, data on changes in T790M in serum; and radiographic and symptom changes along T790Mi therapy were collected. T790M in serum was detected using a PNA-locked nucleic PCR clamp-based technique. T790M was evaluated at baseline and at certain times after T790Mi initiation.
Results:
80% of the p were female and never smoker; 100% were adenocarcinoma, Caucasian, del19, and were treated with previous TKI, with a median (m) time to treatment failure of 11.25 months (mo) [range (r)1-19 mo]. P received 2 previous treatments (r1-6), 40% had a rebiopsy for T790M evaluation, had 3 metastatic sites (r1-6), and had a PS 1 in 70% of the cases. 5 p were evaluable for response with 2 SD and 3 PR as best response (BR) in the 1[st ]evaluation. 7 out of 9 p evaluable for clinical response, experienced an improvement in baseline symptoms as soon as 3 weeks (w) after starting T790Mi, only 1 p experienced an increase in pain, but not related to bone M1. T790M was lost in 80% of the p and it was not detected in serum at 3 or 6 w after the T790Mi initiation in 2 out of 4 and 4 out of 7 evaluable p, respectively.
Conclusion:
T790M detection can be lost early along T790Mi treatment. The decrease in symptom burden is seen in p with loss of T790M. PR and SD represent the BR in p with loss of T790M. The loss of T790M in the serum may be a marker of symptomatic and radiographic response to T790Mi. Future evaluation would demonstrate if the reappearance of T790M mutation in serum could be a marker of resistance to T790Mi.
