470P - Progression-free survival and response rate with EGFR tyrosine kinase inhibitor treatment according to EGFR mutation subtype in advanced lung adeno...

Date 18 December 2016
Event ESMO Asia 2016 Congress
Session Poster lunch
Topics Anticancer Agents
Non-Small-Cell Lung Cancer, Metastatic
Translational Research
Presenter Chee Shee Chai
Citation Annals of Oncology (2016) 27 (suppl_9): ix139-ix156. 10.1093/annonc/mdw594
Authors C.S. Chai1, C.K. Liam2, Y.K. Pang2, K.S. Kow2, C.K. Wong2, M.E. Poh2, J.L. Tan2
  • 1Department Of Medicine, Faculty of Medicine and Health Science, University Malaysia Sarawak, 94300 - Kota Samarahan/MY
  • 2Department Of Medicine, University of Malaya Faculty of Medicine, 59100 - Kuala Lumpur/MY



The presence of epidermal growth factor receptor (EGFR) mutation in advanced lung adenocarcinoma is a strong predictor of EGFR-tyrosine kinase inhibitor (TKI) responsiveness. However, studies regarding predictors of EGFR-TKI responsiveness in EGFR-mutant advanced lung adenocarcinoma are few. This study aimed to determine demographic and clinical factors that affect EGFR-TKI responsiveness in EGFR-mutant advanced lung adenocarcinoma.


Eighty-four patients with EGFR-mutant (except T790M) stage IIIB/IV lung adenocarcinoma with Eastern Cooperative Oncology Group performance status (EPS) of 0-2 treated with first generation EGFR-TKI (gefitinib or erlotinib) in University Malaya Medical Center between August 2010 and July 2014 were retrospectively analyzed.


The median progression free survival (mPFS) was 6.97 months (95% CI, 5.82–8.12) and overall survival was 10.23 months (95% CI, 7.91–12.55) for the 84 patients. The objective response rate (ORR) and disease control rate was 41.7% (95% CI, 31.0–52.4) and 81.0% (95% CI, 72.6–89.3), respectively. Patients with exon 21 L858R point mutation (23 of 28) had the best mPFS (9.27 months), followed by exon 19 deletion mutation (35 of 48) (mPFS = 7.0 months) and exon 18 G719X/exon21 L861Q mutation (3 of 5) (mPFS = 6.0 months). The ORR was 47.9% (23 of 48) for exon 19 deletion, 35.7% (10 of 28) for exon 21 L858R mutation and 40.0% (2 of 5) for exon 18 G719X/exon21 L861Q mutation. Patients with exon 20 S768I/insertion mutation had mPFS of 1.7 months (3 of 3) only and not response to treatment. Multivariate analysis showed that only exon 20 S768I/insertion mutation (HR, 5.63; 95% CI, 1.63–19.45; p = 0.006) was independently associated with poorer PFS. Age, gender, smoking status, stage of disease, EPS and types of first-generation EGFR-TKI had no impact on the mPFS or ORR.


Exon 20 S768I/insertion mutation was an independent predictor of poorer PFS in patients with EGFR-mutant advanced lung adenocarcinoma treated with first generation EGFR-TKI. Randomized control trial using first generation EGFR-TKI in patients with these mutations should be conducted to confirm this finding.

Clinical trial indentification

MECID.NO 201412-871 - medical ethic code from ethic committee of University Malaya Medical Center, Kuala Lumpur, Malaysia.

Legal entity responsible for the study

Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia




All authors have declared no conflicts of interest.