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C. Zhou
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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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129O - EGFR-TKIs plus local therapy demonstrated survival benefit than TKIs alone in EGFR-mutant NSCLC patients with oligometastatic or oligoprogressive liver metastases (ID 166)
16:45 - 18:30 | Author(s): C. Zhou
- Abstract
Background:
Our previous study demonstrated that liver metastases (LM) were the negative predictive and prognostic factor in EGFR-mutant NSCLC patients (Pts) treated with EGFR-TKIs, suggesting that additional treatment is warranted. Recently, several studies reported that local therapy could significantly improve progression-free survival (PFS) in NSCLC Pts with oligometastatic or oligoprogressive disease. This study aimed to investigate whether addition of local therapy to EGFR-TKIs could provide survival benefit in EGFR-mutant NSCLC Pts with oligometastatic or oligoprogressive LM.
Methods:
Pts with EGFR-mutant NSCLC and LM were included. Oligometastatic LM was defined as <5 sites in liver without extrahepatic metastases at initial diagnosis. Oligoprogressive LM was defined as <5 sites in liver without extrahepatic metastases during TKIs therapy. For oligoprogressive cohort, PFS1 was calculated from time of initiation of TKI therapy to first RECIST 1.1 defined progress disease (PD) or death. PFS2 was calculated from time of initiation of TKI therapy to off-TKI PD.
Results:
289 Pts with LM were enrolled (55 with oligometastatic LM and 63 with oligoprogressive LM). In oligometastatic cohort, 18 Pts received EGFR-TKIs (E) and 21 Pts received TKIs plus local therapy (E + LT) as first-line treatment. Median PFS was significantly longer in E + LT group than in E group (12.2 vs. 7.9 m, P = 0.030). Median OS was numerically longer in E + LT group than in E group (31.7 vs. 21.3 m, P = 0.102). In oligoprogressive cohort, 19 Pts received continuation of TKIs plus local therapy (cE + LT) and 22 Pts received switch therapy (ST). Median PFS1 was comparable. Median PFS2 was dramatically longer in cE + LT group than in ST group (13.9 vs. 8.8 m, P = 0.050). Median OS was marginally significantly longer in cE + LT group than in ST group (24.7 vs. 15.7 m, P = 0.085). Multivariate analysis revealed that addition of local therapy was independently associated with prolonged PFS and OS in Pts with oligometastatic LM.
Conclusions:
The current study indicated that EGFR-TKIs plus local therapy demonstrated the prolonged survival benefit than TKIs alone in EGFR-mutant NSCLC Pts with oligometastatic or oligoprogressive LM.
Clinical trial identification:
Legal entity responsible for the study:
Shanghai Pulmonary Hospital
Funding:
Has not received any funding
Disclosure:
All authors have declared no conflicts of interest.
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Poster Display session (Friday) (ID 65)
- Event: ELCC 2018
- Type: Poster Display session
- Track:
- Presentations: 1
- Moderators:
- Coordinates: 4/13/2018, 12:30 - 13:00, Hall 1
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158P - Afatinib in patients with EGFR mutation-positive (EGFRm+) NSCLC harbouring uncommon mutations: Overview of clinical data (ID 567)
12:30 - 13:00 | Author(s): C. Zhou
- Abstract
Background:
Approximately 10–12% of patients with EGFRm+ NSCLC have tumours harbouring uncommon EGFR mutations; however, there is a paucity of clinical data on the sensitivity of these tumours to EGFR TKIs. Preclinical data indicate that the irreversible ErbB family blocker, afatinib, has similar activity against certain uncommon mutations (e.g. L858M/S768I) to that against the common L858R mutation.[1,2]
Methods:
Here, we review the key clinical data available for first-line afatinib in EGFRm+ NSCLC harbouring uncommon EGFR mutations.
Results:
Post-hoc analysis of the randomised LUX-Lung 2/3/6 trials[3] demonstrates that afatinib is clinically active against certain uncommon EGFR mutations. Among 75 afatinib-treated patients with tumours harbouring uncommon mutations in these trials the objective response rate against G719X (n = 18), L861Q (n = 16) and S768I (n = 8) single/compound mutations was 78%, 56% and 100%. Response rate was lower in patients with exon 20 insertions (n = 23; 9%) or de novo T790M (n = 14; 14%). In 38 patients with uncommon mutations/duplications in exons 18–21 PFS was 10.7 months (95% CI 5.6–14.7) and OS was 19.4 months (95% CI 16.4–26.9). The clinical activity of afatinib against uncommon mutations is substantiated by observations outside of the randomised controlled trial setting. In a Phase IIIb single-arm open-label study of afatinib in its registered indication, 67 of 479 TKI-naïve patients had NSCLC with uncommon mutations[4] (exon 20 insertions; L861Q; G719S/A/C; T790M; S768I: 5.2; 4.6; 2.3; 1.0; 1.9%, respectively). Median PFS in these patients was 9.1 months (95% CI 5.6–13.6).[4] In an analysis of 165 EGFRm+ NSCLC patients treated with first-line afatinib in real-world practice in South Korea median PFS in those with uncommon mutations excluding T790M (n = 10) was not reached vs 4.7 months in those with T790M (n = 4; p = 0.01).[5]
Conclusions:
Afatinib has shown preclinical and clinical activity in patients with NSCLC harbouring uncommon EGFR mutations, including G719X, L861Q and S768I. These data could help inform clinical decisions in this patient population. 1. Saxon. J Thorac Oncol 2017;12:884 2. Banno. Cancer Sci 2016;107:1134 3. Yang. Lancet Oncol 2015;16:830 4. Wu. WCLC 2017 P3.01-036 5. Kim. WCLC 2017 P3.01-023
Clinical trial identification:
N/A
Legal entity responsible for the study:
Boehringer Ingelheim
Funding:
Boehringer Ingelheim
Disclosure:
A. Märten: Employment: Boehringer Ingelheim. N. Yamamoto: Membership on an advisory board or board of directors: BI, AZ, Chugai Corporate-sponsored research: BI. C-J. Yu: Membership on an advisory board or board of directors: Roche, ONO, Chugai, Novartis. Y-L. Wu: Honoraria: AstraZeneca, Roche, Eli Lilly, Pfizer, Sanofi. All other authors have declared no conflicts of interest.
