Display options
Share it on

Onco Targets Ther. 2012;5:439-47. doi: 10.2147/OTT.S37289. Epub 2012 Dec 12.

Comparison of different methods for detecting epidermal growth factor receptor mutations in peripheral blood and tumor tissue of non-small cell lung cancer as a predictor of response to gefitinib.

OncoTargets and therapy

Fei Xu, Jingxun Wu, Cong Xue, Yuanyuan Zhao, Wei Jiang, Liping Lin, Xuan Wu, Yachao Lu, Hua Bai, Jiasen Xu, Guanshan Zhu, Li Zhang

Affiliations

  1. State Key Laboratory of Oncology in South China, Department of Medical Oncology, Sun Yat-Sen University Cancer Center, Guangzhou, Guangdong, People's Republic of China.

PMID: 23251095 PMCID: PMC3525047 DOI: 10.2147/OTT.S37289

Abstract

BACKGROUND: Previous studies have reported that epidermal growth factor receptor (EGFR) mutation in tumor tissue and peripheral blood can predict the response to EGFR tyrosine kinase inhibitor (TKI) in non-small cell lung cancer (NSCLC). However, the heterogeneity of the sample sources makes it difficult to evaluate the detecting methodologies. The goal of this study is to compare different methods for analyzing EGFR mutation in blood and tumor tissue.

MATERIALS AND METHODS: Fifty-one advanced NSCLC patients treated with gefitinib were included in the study. The EGFR mutation status of each patients' blood was analyzed by denaturing high-performance liquid chromatography (DHPLC), mutant-enriched liquidchip (ME-Liquidchip), and Scorpion Amplification Refractory Mutation System (Scorpion-ARMS) kits. EGFR mutation information in paired tumor samples detected by Scorpion-ARMS served as a reference. Comparative analyses were performed on mutation status results obtained from different methods and on the association between the clinical outcome of TKI treatment and EGFR mutation status.

RESULTS: The response rate (RR) in the whole group was 33.3%. EGFR mutation rates were identified as 15.7%, 27.5%, and 29.4% by DHPLC, ME-Liquidchip, and Scorpion-ARMS in blood, respectively. In 34 cases that had paired tumor samples, the mutation rate in tissue was 41.2%. The RRs of patients with mutation detected by different methods were 71.4% (tumor), 62.5% (blood, DHPLC), 50.0% (blood, ME-Liquidchip), and 66.7% (blood, Scorpion-ARMS). EGFR mutation detected by Scorpion-ARMS in blood and tumor tissues had better prediction of RR to EGFR-TKI (P = 0.002 and P = 0.001) than mutation detected with DHPLC and ME-Liquidchip.

CONCLUSION: Tumor tissue sample is the best source for EGFR mutation analysis in NSCLC patients. Peripheral blood samples may be used as an alternative source only in special conditions. Scorpion-ARMS, DHPLC, or ME-Liquidchip methods are all optional for detecting tumor EGFR mutation from blood.

Keywords: EGFR mutation; gefitinib; mutation detection methods; non-small cell lung cancer

References

  1. J Clin Oncol. 2009 Dec 20;27(36):6251-66 - PubMed
  2. Ann Oncol. 2010 May;21 Suppl 5:v116-9 - PubMed
  3. J Clin Oncol. 2009 Jun 1;27(16):2653-9 - PubMed
  4. N Engl J Med. 2010 Jun 24;362(25):2380-8 - PubMed
  5. Proc Natl Acad Sci U S A. 2004 Sep 7;101(36):13306-11 - PubMed
  6. Cancer Res. 1993 May 15;53(10 Suppl):2379-85 - PubMed
  7. N Engl J Med. 2009 Sep 3;361(10):958-67 - PubMed
  8. J Clin Oncol. 2005 Nov 1;23(31):8081-92 - PubMed
  9. Crit Rev Oncol Hematol. 1995 Jul;19(3):183-232 - PubMed
  10. Clin Chem Lab Med. 2010 Aug;48(8):1103-6 - PubMed
  11. Science. 2004 Jun 4;304(5676):1497-500 - PubMed
  12. J Thorac Oncol. 2012 Jan;7(1):115-21 - PubMed
  13. N Engl J Med. 2009 Sep 3;361(10):947-57 - PubMed
  14. N Engl J Med. 2005 Jul 14;353(2):123-32 - PubMed
  15. J Clin Oncol. 2003 Jun 15;21(12):2237-46 - PubMed
  16. Br J Cancer. 2007 Sep 17;97(6):778-84 - PubMed
  17. Cancer. 2006 Dec 15;107(12):2858-65 - PubMed
  18. J Clin Oncol. 2005 Apr 10;23(11):2513-20 - PubMed
  19. J Natl Compr Canc Netw. 2010 Jul;8(7):740-801 - PubMed
  20. Clin Cancer Res. 2004 Dec 15;10(24):8195-203 - PubMed
  21. Clin Chem Lab Med. 2011 Feb;49(2):191-5 - PubMed
  22. Zhonghua Bing Li Xue Za Zhi. 2008 May;37(5):294-9 - PubMed
  23. Cancer Res. 2004 Dec 15;64(24):8919-23 - PubMed
  24. J Natl Cancer Inst. 2000 Feb 2;92(3):205-16 - PubMed
  25. N Engl J Med. 2008 Jul 24;359(4):366-77 - PubMed
  26. N Engl J Med. 2005 Jul 14;353(2):133-44 - PubMed
  27. N Engl J Med. 2004 May 20;350(21):2129-39 - PubMed
  28. J Natl Cancer Inst. 2005 Mar 2;97(5):339-46 - PubMed
  29. Clin Chem. 2007 Jan;53(1):62-70 - PubMed
  30. Clin Cancer Res. 2005 Feb 1;11(3):1167-73 - PubMed
  31. Clin Cancer Res. 2006 Jul 1;12(13):3915-21 - PubMed

Publication Types