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Comparison of clinical outcome of patients with non-small-cell lung cancer harbouring epidermal growth factor receptor exon 19 or exon 21 mutations
  1. Young-Woong Won1,
  2. Ji-Youn Han2,3,
  3. Geon Kook Lee2,3,
  4. Seog-Yun Park4,
  5. Kun Young Lim2,
  6. Kyong-Ah Yoon3,
  7. Tak Yun2,
  8. Heung Tae Kim2,3,
  9. Jin Soo Lee2,3
  1. 1Center for Clinical Trials, National Cancer Center Hospital, National Cancer Center, Goyang-si, Republic of Korea
  2. 2Center for Lung Cancer, National Cancer Center Hospital, National Cancer Center, Goyang-si, Republic of Korea
  3. 3Lung Cancer Branch, National Cancer Center Research Institute, National Cancer Center, Goyang-si, Republic of Korea
  4. 4Department of Pathology, National Cancer Center Hospital, National Cancer Center, Goyang-si, Republic of Korea
  1. Correspondence to Ji-Youn Han, Center for Lung Cancer of National Cancer Hospital and Lung Cancer Branch of National Cancer Center Research Institute, National Cancer Center, 323 Ilsan-ro, Ilsandong-gu, Goyang-si, Gyeonggi-do 410-769, Republic of Korea; jymama{at}ncc.re.kr

Abstract

Aims Deletion of exon 19 of the epidermal growth factor receptor (EGFR) and mutation of exon 21 are the most common EGFR mutations and predict higher response to EGFR tyrosine kinase inhibitors (TKI). Accumulating data show clinical differences in both response and survival between these two EGFR mutations. This study investigated the clinical impact of EGFR exon 19 deletion and L858R mutation by retrospectively analysing the clinical outcome of patients with advanced non-small-cell lung cancer (NSCLC) treated with EGFR TKI.

Methods Patients harbouring EGFR exon 19 deletion or L858R mutations and who had received gefitinib or erlotinib treatment were identified. The response rate (RR), progression-free survival (PFS) and overall survival (OS) were determined for the two groups. EGFR mutation was determined by PCR-based direct sequencing.

Results The study indentified 87 patients harbouring EGFR exon 19 deletion (n=61) or L858R mutation (n=26) who were treated with either gefitinib (n=83) or erlotinib (n=4). Patients with exon 19 deletion had significantly longer PFS, compared with patients with L858R mutation (9.3 vs 6.9 months, p=0.02). In a multivariate Cox regression model, EGFR exon 19 deletion was independently predictive of longer PFS (p=0.02). However, no significant differences in RR (64% vs 62%, p=0.83) and OS (17.7 vs 20.5 months, p=0.65) were observed between these two mutations.

Conclusions While no significant difference in OS was observed between EGFR exon 19 deletion and L858R mutation, EGFR exon 19 deletion was predictive of longer PFS following EGFR TKI treatment in patients with advanced NSCLC.

  • Cancer
  • cancer genetics
  • cancer research
  • colorectal cancer
  • cytogenetics
  • epidermal growth factor receptor
  • erlotinib
  • gall bladder
  • gefitinib
  • haematology
  • lung cancer
  • molecular oncology
  • molecular pathology
  • mutation
  • non-small-cell lung cancer
  • oncogenes
  • oncology
  • pancreas

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Footnotes

  • Funding This study was supported in part by NCC (National Cancer Center, Republic of Korea) grant 1110100-1.

  • Competing interests None.

  • Patient consent Obtained.

  • Ethic approval This study was approved by the Institutional Review Board of the National Cancer Center, Republic of Korea (NCCNCS-11-428).

  • Provenance and peer review Not commissioned; externally peer reviewed.

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