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G.L. Laidlaw
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P1.08 - Poster Session with Presenters Present (ID 460)
- Event: WCLC 2016
- Type: Poster Presenters Present
- Track: Surgery
- Presentations: 1
- Moderators:
- Coordinates: 12/05/2016, 14:30 - 15:45, Hall B (Poster Area)
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P1.08-033 - Effect of EGFR Mutations on Survival in Patients following Surgical Resection of Lung Adenocarcinoma (ID 4938)
14:30 - 14:30 | Author(s): G.L. Laidlaw
- Abstract
Background:
While numerous trials have evaluated the effects of EGFR mutations on survival in patients undergoing treatment with tyrosine kinase inhibitors (TKIs), research on the influence of EGFR mutations in patients undergoing surgical resection as their primary intervention is limited and conflicting. We hypothesized that patients with resectable EGFR-mutant tumors have a better postoperative prognosis than those with wild-type (WT) tumors, as EGFR-mutant tumors often include an in-situ component that portends an improved prognosis. We further hypothesized that the two most common EGFR mutations may impact post-resection prognosis differentially.
Methods:
We carried out a single-center, retrospective study evaluating the influence of EGFR mutation status on progression-free (PFS) and overall survival (OS) after resection, adjusting for tumor stage and ethnicity. Kaplan-Meier plots and Cox proportional hazard models were used to generate crude and adjusted hazard ratios.
Results:
249 patients underwent lung adenocarcinoma resection and had mutational analysis and ≥1 year of follow-up at our institution between 2008-2015. These resections included 200 lobectomies, 12 segmentectomies, and 32 wedge resections. Ninety-three (37.3%) patients had EGFR-mutant tumors. Relative to WT tumors, EGFR-mutant tumors were more likely to exhibit well-differentiated (44.0% vs 29.0%, p=0.009) or lepidic (61.3% vs 36.5%, p <0.0001) histology, and trended towards presenting as pathologic stage IA/IB (p=0.082). EGFR mutation improved crude OS (HR 0.39, 95% CI 0.159-0.931, p=0.034), but this difference became nonsignificant when adjusted for tumor stage and ethnicity (OS HR 0.549, 95% CI 0.200-1.508, p=0.245). PFS did not differ between mutant and WT cohorts (adjusted HR 0.94, 95% CI 0.550-1.603, p=0.817). In comparing L858R and Exon 19, neither PFS (adjusted HR 0.91, 95% CI 0.350-2.379, p=0.851) nor OS (HR 0.88, HR 0.160-4.790, p=0.879) significantly differed. Lastly, sublobar resection did not interact with EGFR mutation presence to affect PFS (interaction p-value=0.735) or OS (interaction p-value=0.771).
Conclusion:
Patients with EGFR-mutant adenocarcinomas exhibit improved crude post-resection OS vs. those with WT tumors, but this difference disappears after adjustment for tumor stage and ethnicity. These findings appear attributable to EGFR-mutant tumors presenting at earlier stages. We hypothesize that this occurs because lepidic tumors spend a longer phase in stage I before developing a more aggressive phenotype. Our finding that EGFR mutation status does not interact with resection extent (sublobar vs. ≥ lobar) suggests that mutation status should not affect surgical planning prior to resection.
