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D. Planchard
Moderator of
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Resistance to TKIs (ID 23)
- Event: ELCC 2018
- Type: Educational session
- Track:
- Presentations: 4
- Moderators:T.S.K. Mok, D. Planchard
- Coordinates: 4/13/2018, 11:00 - 12:30, Room B
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Focus on local treatment options (ID 96)
11:00 - 12:30 | Presenting Author(s): F. McDonald
- Abstract
- Presentation
Abstract not provided
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General mechanisms of resistance (ID 93)
11:00 - 12:30 | Presenting Author(s): T. Mitsudomi
- Abstract
- Presentation
Abstract not provided
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Therapeutic strategies to overcome ALK and ROS1 (ID 95)
11:00 - 12:30 | Presenting Author(s): S. Ortiz-Cuaran
- Abstract
- Presentation
Abstract not provided
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Therapeutic strategies to overcome EGFR (ID 94)
11:00 - 12:30 | Presenting Author(s): T.S.K. Mok
- Abstract
- Presentation
Abstract not provided
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Author of
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ESMO-IASLC Best Abstracts (ID 61)
- Event: ELCC 2018
- Type: Best Abstract session
- Track:
- Presentations: 1
- Moderators:M. Perol, L. Paz-Ares
- Coordinates: 4/13/2018, 16:45 - 18:30, Room B
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128O - Osimertinib vs standard of care (SoC) EGFR-TKI as first-line therapy in patients (pts) with untreated EGFRm advanced NSCLC: FLAURA post-progression outcomes (ID 570)
16:45 - 18:30 | Presenting Author(s): D. Planchard
- Abstract
- Presentation
Background:
In the FLAURA phase 3 study, the third-generation EGFR-TKI osimertinib significantly improved progression-free survival (PFS) vs SoC EGFR-TKIs (gefitinib or erlotinib) in pts with previously untreated Ex19del/L858R (EGFRm) advanced NSCLC (hazard ratio [HR] 0.46 [95% CI 0.37, 0.57]; p < 0.001). Interim overall survival (OS) data was encouraging but not formally statistically significant (HR 0.63 [95% CI 0.45, 0.88]; p = 0.007). Here we report exploratory post-progression outcomes.
Methods:
Pts were randomised 1:1 to receive osimertinib (80 mg orally [PO], once daily [QD]) or SoC (gefitinib 250 mg PO QD or erlotinib 150 mg PO QD). Treatment beyond disease progression was allowed if the investigator judged continued clinical benefit; investigators determined subsequent therapy. Pts receiving SoC could cross over to osimertinib after objective disease progression with documented post-progression T790M-positive mutation status.
Results:
At data cutoff, 12 June 2017, 138/279 (49%) and 213/277 (77%) pts discontinued osimertinib and SoC, respectively; 82 (29%) and 129 (47%) received a subsequent treatment: EGFR-TKI-containing, 29 (10%) and 97 (35%; 55 [20%] osimertinib); platinum chemotherapy-containing, 46 (16%) and 27 (10%). Median time (mths) to discontinuation of study treatment or death: osimertinib 20.8 (95% CI 17.2, 24.1) vs SoC 11.5 (10.3, 12.8). Median time (mths) to discontinuation of any EGFR-TKI (study treatment and subsequent EGFR-TKI, not interrupted by non-EGFR-TKI therapy) or death: osimertinib 23.0 (19.5, not calculable [NC]) vs SoC 16.0 (14.8, 18.6). Time-to-event post-progression endpoints all favoured osimertinib (Table).
aCalculated using the Kaplan-Meier method.bHR and CI were obtained directly from the U and V statistics. The analysis was performed using a log rank test stratified by race (Asian versus non-Asian) and mutation type (Ex19del vs L858R). 2-sided p-value. CI, confidence interval; FST, first subsequent therapy (second-line treatment); HR, hazard ratio; NC, not calculable; PFS2, second progression-free survival (or death) post initiation of second-line treatment (i.e. time from randomisation to second progression on subsequent treatment); TFST, time to first subsequent therapy or death; TSST, time to second subsequent therapy or death; SST, second subsequent therapy; RECIST, Response Evaluation Criteria In Solid Tumors version 1.1.Osimertinib(n = 279) SoC (n = 277) Disease progression or death, n (%) 136 (49) 206 (74) Remained on study treatment for at least 7 days post investigator assessed progression, n/N (%) 91/136 (67) 145/206 (70) Median duration on study treatment post-progression (95% CI), wks[a] 8.1 (6.3, 12.3) 7.0 (5.9, 8.1) TFST Pts who started FST or died, n (%) 115 (41) 175 (63) Started FST, n (%) 82 (29) 129 (47) Died, n (%) 33 (12) 46 (17) Median TFST or death (95% CI), mths[a] 23.5 (22.0, NC) 13.8 (12.3, 15.7) HR (95% CI)[b] 0.51 (0.40, 0.64), p < 0.0001 PFS2 (investigator assessed) Second progression or death, n (%) 73 (26) 106 (38) Median PFS2 (95% CI), mths[a] NC (23.7, NC) 20.0 (18.2, NC) HR (95% CI)[b] 0.58 (0.44, 0.78), p = 0.0004 TSST Pts who started SST or died, n (%) 74 (27) 110 (40) Started SST, n (%) 24 (9) 39 (14) Died, n (%) 50 (18) 71 (26) Median TSST or death (95% CI), mths[a] NC (NC, NC) 25.9 (20.0, NC) HR (95% CI)[b] 0.60 (0.45, 0.80), p = 0.0005
Conclusions:
PFS benefit with osimertinib was preserved throughout time-to-event post-progression endpoints. Step-wise increase of the statistically significant HRs (PFS 0.46, TFST 0.51, PFS2 0.58, TSST 0.60) provides confidence in the interim OS data.
Clinical trial identification:
ClinicalTrials.gov NCT02296125
Legal entity responsible for the study:
AstraZeneca
Funding:
AstraZeneca
Disclosure:
D. Planchard: Advisory boards: Astrazeneca, Boehringer, BMS, Pfizer, Novartis, MSD, Roche M. Boyer: Research funding and/or honoraria for advisory board work or talks, paid to my institution, from: AstraZeneca, Roche, Merck Sharpe and Dohme, Pfizer, Amgen, Bristol-Myers Squibb. P. Cheema: Advisory board/Honorarium: AstraZeneca Research grant: AstraZeneca T. Takahashi: Honoraria: AstraZeneca, Eli Lilly Japan, Chugai Pharmaceutical, Ono Pharmaceutical, Grants: AstraZeneca KK, Pfizer Japan Inc., Eli Lilly Japan K.K., Chugai Pharmaceutical Co., Ltd., Taiho Pharmaceutical Co., Ltd., MSD K.K. A. Todd: Employee of AstraZeneca but own no stocks or shares, and am not a member of any board. I am not aware of any other conflicts of interest or opportunities for financial gain. A. McKeown: Employee of, and shareholder in, AstraZeneca. Y. Rukazenkov: Employee of and shareholder in AstraZeneca. Y. Ohe: Grants and personal fees from AstraZeneca, during the conduct of the study; grants and personal fees from AstraZeneca, grants and personal fees from Ono, grants and personal fees from BMS, grants and personal fees from Chougai, grants and personal fees from Pfizer, grants and personal fees from MSD, grants and personal fees from Novartis, grants from Kyorin, grants from Dainippon- Sumitomo, personal fees from Daiichi-Sankyo, personal fees from Nipponkayaku, personal fees from Boehringer Ingelheim, personal fees from Bayer, grants and personal fees from Lilly, outside the submitted work. All personal fees were honoraria for consulting or lectures. All other authors have declared no conflicts of interest.
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Guiding the best targeted treatment (ID 27)
- Event: ELCC 2018
- Type: Multidisciplinary Tumour Board
- Track:
- Presentations: 1
- Moderators:E. Smit, F. Lopez-Rios
- Coordinates: 4/13/2018, 14:45 - 16:15, Room A
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Progression on osimertinib: When is it possible to continue with a targeted therapy? (ID 111)
14:45 - 16:15 | Presenting Author(s): D. Planchard
- Abstract
- Presentation
Abstract not provided
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Immunotherapy and next-generation TKIs: From second to frontline treatment (ID 55)
- Event: ELCC 2018
- Type: Poster Discussion session
- Track:
- Presentations: 1
- Moderators:P. Garrido Lopez, S. Ekman, S. Ortiz-Cuaran, E. Wauters
- Coordinates: 4/12/2018, 07:45 - 09:00, Room A
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144PD - Leptomeningeal metastases in EGFR-mutated non-small cell lung carcinoma: Management after tyrosine kinase inhibitors (ID 611)
07:45 - 09:00 | Author(s): D. Planchard
- Abstract
Background:
Leptomeningeal metastases (LM) in non-small-cell lung carcinoma (NSCLC) are associated with poor outcome. Tyrosine kinase inhibitors (TKIs) are active in LM+ EGFR mutated (EGFRm) patients (pts), but optimal patient's management after failure of TKIs is unknown.
Methods:
We included consecutive pts with EGFRm NSCLC who had LM progression during first-line EGFR TKI, defined as diagnosis of LM during TKI treatment or progression of known LM after first-line TKI, treated in our institution. Clinical and pathological data were retrospectively collected. We evaluated overall survival (OS), progression-free survival (PFS), clinical response rate (CRR), and disease control rate (DCR) defined as clinical response or stable disease >2 months.
Results:
We included 66 pts treated between Apr. 2003 and Sept. 2016, with a median age of 54 years [26–79]; 51 (77%) were females; 56 (85%) non-smokers. Twenty-three tumors (35%) had exon 19 deletion, 23 (35%) L858R exon 21 mutation, 10 (15%) T790M mutation. Median number of previous lines was 2 [1–7], and 19 pts (29%) had additional intrathecal treatment. 2[nd] line TKI was given to 36 pts (55%): 19 (53%) received erlotinib, 10 (28%) high dose (HD) erlotinib (300 mg daily), 3 osimertinib, 4 other 1[st]/2[nd] generation TKI (3 gefitinib, 1 afatinib). Median PFS and OS from LM progression were 3 months (m) [CI95% 2–3] and 7 m [CI95% 3–16], respectively. CRR and DCR for 2nd-line TKI were 43% and 77%. Nine pts (25%) were alive at 10 m (6 erlotinib, 1 HD erlotinib, 2 osimertinib). Median OS for erlotinib, HD erlotinib, osimertinib and other 1[st]/2[nd] generation TKI were 8 m (CI 95% 7–16), 3 m (CI 95% 2-not reached (NR)), NR (CI 95% NR-NR), and 2.5 m (CI 95% 0-NR), respectively. Patients treated with erlotinib, of whom 79% received prior afatinib or gefitinib, had better OS compared to patients treated with other 1[st]/2[nd] generation TKI (8 m vs. 2.5 m, P = 0.04). CRR and DCR in patients with HD erlotinib were 40% and 60%, respectively, of whom 80% received prior erlotinib.
Conclusions:
2[nd]-line TKI can increase survival in LM+ EGFRm NSCLC previously treated with TKI. Sequential erlotinib after prior gefitinib or afatinib seems to be a suitable strategy. Increasing erlotinib dose has demonstrated clinical benefit.
Clinical trial identification:
Legal entity responsible for the study:
Gustave Roussy
Funding:
Has not received any funding
Disclosure:
All authors have declared no conflicts of interest.
