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Toyoaki Hida
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EP1.01 - Advanced NSCLC (ID 150)
- Event: WCLC 2019
- Type: E-Poster Viewing in the Exhibit Hall
- Track: Advanced NSCLC
- Presentations: 1
- Now Available
- Moderators:
- Coordinates: 9/08/2019, 08:00 - 18:00, Exhibit Hall
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EP1.01-32 - Improving the Prognosis of Non-Small Cell Lung Cancer After the Approval of Immune Checkpoint Inhibitors: A Retrospective Analysis (Now Available) (ID 1276)
08:00 - 18:00 | Author(s): Toyoaki Hida
- Abstract
Background
Anti-programmed death-1/programmed death-ligand-1 (PD-1/PD-L1) blockade represents a revolutionary breakthrough in the treatment of advanced non-small-cell lung cancer (NSCLC). However, it remains unclear whether the immunotherapy for PD-1 axis are associated with overall survival (OS) in real world patients.
Method
We retrospectively analyzed consecutive 246 patients with stage IIIB or IV NSCLC who underwent at least 1 regimen of chemotherapy. Patients who have EGFR mutations, ALK/ROS1 rearrangements, or received curative thoracic radiotherapy were excluded. Besides, patients administered any immune checkpoint inhibitors in clinical trials were also excluded. Treatment outcomes were compared between patients who started chemotherapy from January 2012 to December 2014 (cohort A; n=135) and those who started it from January 2016 to December 2017 (cohort B; n=111). Baseline characteristics were balanced using propensity score matching, including variables such as age, sex, performance status (PS), histology, clinical stage, bone metastases, central nervous system (CNS) metastases, liver metastases, pulmonary metastases, and pleural dissemination.
Result
Median OS was 11.4months in cohort A and 16.6mo in cohort B (HR 0.68, 95%CI 0.50-0.93, P=0.016). In 111 propensity-score matching pairs, median OS was 11.2months in cohort A and 16.6months in cohort B (HR 0.68, 95%CI 0.49-0.94, P=0.021), and the 12-month OS rate was 48.7% in cohort A versus 59.9% in cohort B, respectively. PD-1 axis inhibitors were received 13.5% in cohort A and 64.9% in cohort B. Forest plot for the propensity-matched patient analysis demonstrated a significantly better outcome in cohort B, for patients with PS 0 to 1, smokers, number of metastases ≤1, no bone metastases, no CNS metastases, no liver metastases, no pulmonary metastases, pleural metastases, and squamous histology.
Conclusion
This result indicates the appearance of immunity checkpoint inhibitors improved the prognosis of driver-mutation negative NSCLC in real world.
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EP1.14 - Targeted Therapy (ID 204)
- Event: WCLC 2019
- Type: E-Poster Viewing in the Exhibit Hall
- Track: Targeted Therapy
- Presentations: 1
- Now Available
- Moderators:
- Coordinates: 9/08/2019, 08:00 - 18:00, Exhibit Hall
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EP1.14-44 - Lung Adenocarcinoma with a Rare BRAF V600E K601_W604del Mutation Responded to Dabrafenib Plus Trametinib Treatment: A Case Report (Now Available) (ID 1485)
08:00 - 18:00 | Author(s): Toyoaki Hida
- Abstract
Background
BRAF V600E mutation can be detected in 1% of lung adenocarcinomas, and far more rarely, complex mutations in addition to BRAF V600E have been reported.
Method
Case presentation: A 42-year-old man was diagnosed with advanced lung adenocarcinoma with stage cT1cN3M1c stageIVB. BRAF V600E mutation was found with in-house molecular testing, so we submitted the same specimen to be analyzed with Oncomine Dx Target test for reimbursement of the subsequent treatment. However, the result was negative for BRAF V600E.
Result
The patient was treated with pembrolizumab (first-line therapy) and then carboplatin, pemetrexed and bevacizumab (second-line therapy). Nevertheless, the disease was progressed, so dabrafenib plus trametinib were used for the third line therapy. One month later CT scan showed a partial response. A subsequent study showed that the V600E mutation accompanied K601_W604 deletion, three bases after the V600E point mutation.
Conclusion
Our clinical experience suggested that some tumors with compound BRAF mutations, such as BRAF V600E K601_W604 del mutation, could respond to dabrafenib plus trametinib treatment, and that rare compound mutations, like this case, may not be detected with the conventional amplicon sequencing, particularly when the additional alterations are acquired at the positions adjacent to hotspots.
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MA21 - Non EGFR/MET Targeted Therapies (ID 153)
- Event: WCLC 2019
- Type: Mini Oral Session
- Track: Targeted Therapy
- Presentations: 1
- Now Available
- Moderators:Benjamin Besse, Michael Thomas
- Coordinates: 9/10/2019, 14:30 - 16:00, Vienna (2016)
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MA21.08 - Discussant - MA21.05, MA21.06, MA21.07 (Now Available) (ID 3807)
14:30 - 16:00 | Presenting Author(s): Toyoaki Hida
- Abstract
- Presentation
Abstract not provided
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OA12 - Profiling the Multidisciplinary Management of Stage III NSCLC (ID 144)
- Event: WCLC 2019
- Type: Oral Session
- Track: Treatment of Locoregional Disease - NSCLC
- Presentations: 1
- Now Available
- Moderators:Dirk De Ruysscher, Bartomeu Massuti
- Coordinates: 9/09/2019, 15:45 - 17:15, Seoul (2007)
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OA12.02 - Randomized Phase II Study of CDDP+S-1 vs CDDP+PEM Combined with Thoracic RT for Locally Advanced Non-Sq NSCLC: SPECTRA Study (Now Available) (ID 428)
15:45 - 17:15 | Author(s): Toyoaki Hida
- Abstract
- Presentation
Background
SPECTRA, a multicenter, randomized phase II study of CDDP+S-1 versus CDDP+pemetrexed (PEM) combined with thoracic radiotherapy (TRT) for locally advanced non-squamous non-small cell lung cancer (NSCLC), previously reported that toxicities were tolerable and manageable in both arms; however, febrile neutropenia was more frequently observed in the CDDP+S-1 arm (9.6%/2%). Completion rate of TRT (60Gy) and chemotherapy (4 cycles) was 92%/98% and 73%/86%, respectively. Response rate was 60%/64% (WCLC 2017, MA17.06). Here, we present primary analysis of 2-year survival data.
Method
Patients were randomly assigned to receive CDDP+S-1 (CDDP 60mg/m2, d1, and S-1 80mg/m2, d1-14, q4w, up to 4 cycles) or CDDP+PEM (CDDP 75mg/m2, d1, and PEM 500mg/m2, d1, q3w, up to 4 cycles) combined with TRT 60Gy in 30 fractions. The primary endpoint was 2-year progression-free survival (PFS) rate. The sample size was set at 100 patients.
Result
Between Jan 2013 and Oct 2016, 102 patients were enrolled in this study from 9 institutions in Japan. All 102 patients were eligible and assessable, of whom 52 were assigned to CDDP+S-1 and 50 to CDDP+PEM. Baseline characteristics were similar (CDDP+S-1/CDDP+PEM): median age (range) 64.5 (39-73)/63.5 (32-74) years; women, n=17 (33%)/n=17 (34%); stage IIIB, n=21 (40%)/n=20 (40%); ECOG PS of 1, n=14 (27%)/n=14 (28%); never smoker, n=12 (23%)/n=12 (24%); and adenocarcinoma, n=47(90%)/n=45(90%); activating EGFR mutation, n=9 (17%)/n=4 (8%); ALK fusion, n=2 (4%)/n=3 (6%). A total of 72 PFS events were observed at the data cut-off (28 November 2018). After a median follow-up of 32.1 months, median PFS was 12.7/13.8 months (HR=1.16, 95% CI, 0.73-1.84, p=0.538), and 2-year PFS rate was 36.5% (95% CI, 23.5-49.6)/32.1% (95%CI, 18.9-45.4). Disease progression was observed in 33 and 36 patients. Distant metastases were the first site of failure in 24 and 31 patients. Local relapse as the first site of failure was observed in 14 and 13 patients. After a median follow-up of 34.6 months, 44 OS events were observed. Median OS was 48.3/59.1 months (HR=1.05, 95%CI, 0.58-1.90, p=0.883), and 2-year OS rate was 69.2% (95%CI, 56.7-81.8)/66.4% (95%CI, 53.0-79.9). 27 patients in each arm received post-study chemotherapy including EGFR-TKIs (n=7/n=5), ALK-TKIs (n=0/n=3), and immune checkpoint inhibitors (n=6/n=10).
Conclusion
2-year PFS rate in the CDDP+S-1 arm was better than that in the CDDP+PEM arm. We will select the CDDP+S-1 arm as the investigational arm in a future phase III study. UMIN000009914 (release date: 31/Jan/2013)
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P2.14 - Targeted Therapy (ID 183)
- Event: WCLC 2019
- Type: Poster Viewing in the Exhibit Hall
- Track: Targeted Therapy
- Presentations: 1
- Moderators:
- Coordinates: 9/09/2019, 10:15 - 18:15, Exhibit Hall
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P2.14-11 - Retreatment with EGFR-TKI for 541 NSCLC Patients with EGFR Mutation (ID 2633)
10:15 - 18:15 | Author(s): Toyoaki Hida
- Abstract
Background
Epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitor (TKI) is remarkably effective against non-small cell lung cancer (NSCLC) harboring EGFR activating mutation. However, tumors almost inevitably develop resistance approximately after one year of EGFR-TKI treatment. In addition, some patients can not tolerate an EGFR-TKI treatment because of adverse events and result in discontinuation of the treatment. In such cases, the same or other EGFR-TKI may be re-administered. However, its efficacy is not fully evaluated.
Method
We retrospectively investigated patients who received EGFR-TKI between January 2008 and August 2017. Among these patients, the response rate and time to treatment failure (TTF) for each re-administered TKI were assessed. We assessed each TTF for patients who discontinued the prior EGFR-TKI because of progressive disease (PD group) and patients who discontinued TKI because of adverse events (AE group). We also evaluated the overall survival (OS) for the patients who received the retreatment with EGFR-TKI and who did not.
Result
A total of 1400 patients from 11 institutions were enrolled in this study. Among them, 570 patients received retreatment with EGFR-TKI, and 541 were eligible. Among the 395 patients who discontinued prior EGFR-TKI because of disease progression, the response rate and the median TTF of subsequent Gefitinib/Erlotinib/Afatinib were 8%/8%/18%, and 4.9/3.2/4.3 months, respectively. The median TTF for the AE group was significantly longer than that for the PD group (10.8 months vs 3.8 months, p<0.0001). In the AE group, The OS for patients receiving retreatment with EGFR-TKI was significantly better than the OS for patients without retreatment (Hazard Ratio = 0.256, p < 0.0001). Similarly, in the PD group, the OS for patients receiving retreatment with EGFR-TKI was significantly better than the OS for patients without retreatment (Hazard Ratio = 0.456, p < 0.0001).
Conclusion
Retreatment with EGFR-TKI was shown to be effective for both patients who discontinued prior EGFR-TKI because of disease progression as well as adverse events.
