6P - Screening for the prevalence of EGFR and ALK mutations in lung adenocarcinoma patients in the Levant area, a prospective analysis

Date 17 April 2015
Event ELCC 2015
Session Poster lunch
Topics Cancer Aetiology, Epidemiology, Prevention
Lung and other Thoracic Tumours
Pathology/Molecular Biology
Presenter Arafat Tfayli
Citation Annals of Oncology (2015) 26 (suppl_1): 1-5. 10.1093/annonc/mdv043
Authors A. Tfayli1, M. Khalil2, A. Mina3, H. Rafei3, N. Fakhreddin4, R. Mahfouz5, F. Farhat6, S. Hamouri7, H. Dbouk8, G. Zaatari5
  • 1Internal Medicine- Hematology-oncology, American University of Beirut Medical Center (AUBMC), 11-0236 - Beirut/LB
  • 2Internal Medicine, University of Miami Miller-West-Palm Beach, Miami/US
  • 3Internal Medicine, American University of Beirut Medical Center, Beirut/LB
  • 4Internal Medicine, Hammoud Hospital University Medical Center, Beirut/LB
  • 5Pathology And Lab Medicine, American University of Beirut Medical Center (AUBMC), Beirut/LB
  • 6Internal Medicine, Hammoud Hospital, Saida/LB
  • 7Internal Medicine- Hematology Oncology, Jordan University of Science and Technology, Irbid/JO
  • 8Internal Medicine- Hematology Oncology, Jabal Amel Hospital, Tripoli/LB



Recent evidence suggests that a significant percentage of lung adenocarcinomas have a driver mutation that is responsible for the development of the tumor and promotion of its growth and spread. Significant variation in the prevalence of these mutations has been documented with race and smoking status being two major factors (more common in Asians and/or non-smokers). To date, no data has prospectively assessed the prevalence of these mutations in a Middle Eastern population and that will be the aim of our study.


Patients with lung adenocarcinoma were prospectively enrolled as part of a multicenter, multinational study. Tumors were tested for various EGFR mutations in exons 18-21 by PCR and for EML4-ALK translocation by FISH Break-Apart test. Study was open in 10 sites in Lebanon, Jordan, and Iraq and was restricted to patients of Middle Eastern origin.


180 patients have been recruited so far. 120 (67%) males and 60 females (33%) with a mean age of 62.6 years. EGFR testing was done in 166 patients and has been found to be Wild type in 142 (85.6%) patients, and mutated in 24 (14.4%). Tissue has been insufficient in 12 (6.7%) of the samples and 2 (1.1%) of the results are still pending. As for the EML4-ALK translocation, it has been tested in 115 patients. Results were negative in 112 (97.4%) patients and positive in 3 (2.6%). 21 attempts at ALK testing failed (11.7%) while the remainder of results are either pending (6 (3.4%)), unattainable due to insufficient tissue (12(6.7%)) or undone because patients were either EGFR or KRAS mutation positive (26(14.4%)).


Because of overwhelming evidence in favor of the survival benefits of targeted therapies, assessing the prevalence of clinically significant mutations has become a must. Although the frequencies of such mutations (KRAS, EGFR, ALK …) have been well established in Western populations, our study will be the first to establish their frequencies in the Levant area. Preliminary results have shown an EGFR mutation rate of 14.4% and an ALK translocation rate of 2.6% in our patient population as compared to a 15-20% and 5% in western literature respectively.


All authors have declared no conflicts of interest.