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Jennifer J Morrissette
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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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P2.14-26 - Outcomes in Patients with Compound Epidermal Growth Factor Receptor (EGFR) Mutations After Treatment with Tyrosine Kinase Inhibitors (TKIs) (ID 1090)
10:15 - 18:15 | Author(s): Jennifer J Morrissette
- Abstract
Background
TKIs targeting EGFR have changed the therapeutic paradigm for patients (pts) with non-small cell lung cancer (NSCLC) harboring classic sensitizing mutations in EGFR (L858R and Exon 19del). Less is known about the efficacy of TKIs when a sensitizing mutation is co-existent with another, not resistance-associated EGFR mutation (compound EGFR mutations). We report the outcomes of pts with de novo compound EGFR mutations treated with TKIs.
Method
We identified pts with compound EGFR mutated NSCLC (plasma or tissue detection) treated at a single center. All disease-associated EGFR mutations were included with the exception of T790M and C797S. Time to treatment failure (TTF) was calculated from the start of TKI therapy until treatment discontinuation for any reason (i.e. disease progression, toxicity, pt choice or death). Overall survival (OS) was calculated from the start of TKI until death. Median OS (mOS) and TTF (mTTF) were estimated from Kaplan-Meier curves.
Result
24 pts with compound EGFR mutations were identified (median age 60, 67% female, 29% never smokers) between 2011 and 2018 (Table 1). Of the 16 (67%) who received a TKI, the most common mutation was G719X (n=9). Exon 19 deletions (del) were present in 2 patients (1 with G719X). L858R was found in 5 patients. Of the 8 pts who did not receive a TKI, 4 had early stage NSCLC that never progressed, 2 had local recurrence treated with surgery/radiation and 2 had metastatic recurrence. Among those treated with a TKI, the mTTF was 13.6 months (mo) and mOS was 32.7 mo. There was no difference in mTTF between erlotinib (n=10) and afatinib (n=6) (13.6 vs. 8.8 mo, log rank p=0.67). Median follow up was 33 mo. In 7 pts who had both baseline tissue and plasma testing, plasma detected all non-classic mutations.
Conclusion
The mOS and mTTF in this cohort of pts with compound EGFR mutations compare favorably to the historical progression free survival and mOS for pts with classic sensitizing mutations in EGFR treated with erlotinib or afatinib.
Table 1: Compound EGFR mutations (n=24)
Exon 3
Exon 18
Exon 19
Exon 20
R108K
E709X
del
S768I
V769M
R776H
Exon 18
G719X
5
1
8
1
1
Exon 19
del
1
Exon 21
L858R
3
2
L861Q
1
1