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A. Feyereislova
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P3.01 - Advanced NSCLC (ID 621)
- Event: WCLC 2017
- Type: Poster Session with Presenters Present
- Track: Advanced NSCLC
- Presentations: 2
- Moderators:
- Coordinates: 10/18/2017, 09:30 - 16:00, Exhibit Hall (Hall B + C)
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P3.01-040 - Real-World Management of Patients with EGFR Mutation-Positive NSCLC in the US (ID 9408)
09:30 - 09:30 | Author(s): A. Feyereislova
- Abstract
Background:
Clinical trials have demonstrated the efficacy and safety of EGFR tyrosine kinase inhibitors (TKIs), as first-line therapy in patients with metastatic non-small-cell lung cancer (NSCLC) whose tumours harbour activating mutations in the EGFR gene. However, there are limited data in the real-world setting describing TKI use among patients with EGFR-mutated NSCLC.
Method:
A retrospective non-interventional study was conducted using the Flatiron Health database, a longitudinal database containing electronic health record data, of patients seen in over 265 United States cancer clinics (~800 sites of care). Adult patients with histologically confirmed stage IIIB or IV NSCLC, with documented EGFR-mutated disease (del 19 or L858R), and who had received the first sequence of systemic therapy between January, 2011 and March, 2016 were included. Patient demographic and clinical disease characteristics were analysed and time-to-next treatment (TTNT) was used as a surrogate measure for progression-free survival. If validated in time, overall survival data will be presented.
Result:
Overall 20,924 adult patients with advanced NSCLC were identified, of whom 12,148 (58.1 %) were tested for EGFR mutations. Among these, 1,919 (15.8 %) patients had a positive EGFR result with 1,412 patients carrying del 19 or exon 21 mutations. Of these, 886 patients were treated with regimens in the first-line setting. Median age was 69.0 years; 67.7% were female; 55.5% were Caucasian; 54.3% were non-smokers; 97.5% had non-squamous histology and 57.3% received at least one subsequent treatment. Most patients received a TKI (71.8%) and 28.2% received other therapy. There were no differences observed in a patient’s type of insurance and the type of treatment (TKI or chemotherapy) that they were likely to receive. Patients treated with an EGFR TKI had a significantly longer median TTNT [erlotinib (13.2 months [95% CI 12.2–14.4; p=<0.001]) afatinib (12.6 months [95% CI 8.6–16.2; p=<0.001]), gefitinib (not evaluable; due to small sample size n=9) than those treated with other anti-cancer agents (4.6 months [95% CI 4.0–5.4]).
Conclusion:
These real world data mirror the results shown in randomised clinical trials, with the exception of patients being generally older. Importantly, patients who did not receive a TKI had significantly shorter TTNT. A large proportion of patients (42%) are not being tested for EGFR mutations, although there was an improvement over time. The reasons for not testing all eligible patients for EGFR mutations should be investigated further.
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P3.01-044 - Erlotinib vs Chemotherapy in EGFR Mut+ NSCLC: OS in Three Phase III Trials Adjusting for Post-Progression Treatment Crossover (ID 9462)
09:30 - 09:30 | Author(s): A. Feyereislova
- Abstract
Background:
In EURTAC, ENSURE and OPTIMAL, first-line erlotinib was associated with higher response rates and improved PFS versus chemotherapy in EGFR Mut+ NSCLC. OS benefit was not observed, possibly due to high crossover. We present statistical analyses of OS adjusting for crossover in the three studies.
Method:
Rank Preserving Structural Failure Time (RPSFT) analysis is a retrospective statistical methodology that estimates the effect of active treatment and then removes that effect from the control patients, during the period of active treatment. Separately, post-hoc OS analyses were conducted on non-randomized subgroups of patients who received a single line of therapy, chemotherapy only or erlotinib only; or a sequence, chemotherapy followed by TKI or erlotinib followed by chemotherapy. Impact of sequencing on OS was evaluated (Kaplan-Meier methodology).
Result:
RPSFT analyses (Table) show OS was numerically longer with erlotinib versus chemotherapy in EURTAC and ENSURE. OS was not longer with erlotinib in OPTIMAL, possibly due to low treatment adherence in the erlotinib arm, where >50% of patients refused chemotherapy or did not complete four cycles. In the non-randomized analyses, patients receiving erlotinib as the sole treatment had longer OS versus patients treated with only chemotherapy, in all three studies. Patients who received erlotinib followed by chemotherapy had longer OS versus patients who received chemotherapy followed by erlotinib in EURTAC and ENSURE. Patients who received chemotherapy followed by erlotinib in OPTIMAL had longer OS than patients who received erlotinib then chemotherapy, again possibly due to erlotinib patients refusing the full extent of post-progression chemotherapy.
Conclusion:
RPSFT analysis showed increased OS between erlotinib and chemotherapy in EURTAC and ENSURE versus the original ITT analysis. Similar impact in OPTIMAL was not apparent. Post-hoc analysis of non-randomized subgroups (patients treated with a single therapy) showed longer OS for erlotinib versus chemotherapy, notwithstanding caveats of such an approach.OS (RPSFT analysis) Study Treatment Group N Median OS, months HR (95% CI) EURTAC Erlotinib 86 22.9 0.64 (0.44, 0.95) Chemo 88 15.4 ENSURE Erlotinib 110 26.3 0.47 (0.32, 0.69) Chemo 107 17.1 OPTIMAL Erlotinib 82 22.7 1.78 (1.21, 2.64) Chemo 72 30.5 Influence of sequencing on OS in patients who crossed over (Kaplan-Meier analysis) Study Treatment Group N Patients crossing over, % Median OS, months EURTAC Erlotinib/chemo 49 57 24.9 Chemo/TKI 72 82 22.6 Erlotinib alone 37 17.2 Chemo alone 16 1.6* ENSURE Erlotinib/Chemo 69 63 27.0 Chemo/TKI 89 83 25.6 Erlotinib alone 41 23.2 Chemo alone 18 22.9 OPTIMAL Erlotinib/ Chemo 49 60 26.8 Chemo/TKI 52 72 31.4 Erlotinib alone 33 18.6 Chemo alone 20 11.2 *There were 5 deaths and 5 censored observations that occurred in the first two months
