Abstract 932: Somatic EGFR mutations and oncogenic viruses in NSCLC Egyptian patients
Authors: Shaimaa Saeed, Amira Salah El-Din Youssef, Ahmed M. Fahmy, Nasra F. Abdel Fattah, Zeinab K. Hassan, Mohamed M. Hafez
Journal: Cancer Research (2025)

Abstract Background: Lung cancer (LC) is the leading cause of cancer-related mortality worldwide, with non-small cell lung cancer (NSCLC) accounting for approximately 75-80% of cases. Genetic alterations, particularly somatic mutations in the Epidermal Growth Factor Receptor (EGFR) gene, play a critical role in NSCLC tumorigenesis and treatment responsiveness. Oncogenic viruses, such as Human Papillomavirus (HPV) and Epstein-Barr virus (EBV) as environmental factors, have also been implicated in various cancers including lung cancer. This study aimed to investigate EGFR somatic mutations profile and its association with theses oncogenic viruses in NSCLC Egyptian patients, hoping to provide new insights on role of EGFR mutations associated with oncogenic viruses in lung cancer development. Methods: This study was conducted on ninety-three formalin-fixed, paraffin-embedded (FFPE) samples of NSCLC Egyptian patients, as well as ten FFPE from safety margins served as control group. The somatic EGFR mutations in exon 18(G719A\G719C and G719S), exon 19(19 deletion), exon 20 (insertions, T790M, S768I), and exon 21(, L858R and L861Q) were detected using AmoyDx® EGFR 29 Mutations Detection Kit. Moreover, the HPV DNA was detected by common primers (MY09 and MY11) targeting the L1 gene using conventional PCR assay. The EBV DNA was detected using the Artus EBV TM PCR Kit, targeting the EBNA 1 gene by real-time PCR. Results: Our results revealed that the EGFR mutations were detected in 19 out of 93 NSCLC patients (20.4%); these mutations were distributed in exon 18 (9.5%), exon 19 (42.8%), exon 20 (28.5%), and exon 21(19%). On the other hand, no mutations were detected in the control group. The total number of EGFR mutations was 21 per 19 NSCLC patients; where all EGFR-mutated NSCLC patients had one mutation, except for two patients had two mutations. The most frequent detected EGFR mutations in NSCLC patients were; 19 del (42.8%), T790M (23.8%), L858R (19%), G719S (9.5%), and insertions (4.7%). Furthermore, the DNA of HPV and EBV were detected in 29 (31.1%) and 2 (2.1%) of NSCLC patients, respectively. On the other hand, these viruses were not detected in the control group. Regarding association of oncogenic viruses with somatic EGFR Mutations, 26.3% were positive for HPV DNA among EGFR-mutated NSCLC patients. No EBV DNA was detected in the EGFR-mutated NSCLC patients (0%). Conclusion: Our findings show that EGFR mutations in conjunction with certain oncogenic viruses, may contribute to the pathogenesis among Egyptian NSCLC patients, however a larger sample size is needed to confirm these findings. The prognosis of EGFR-TKI treatment may vary according to different EGFR actionable mutations and the co-presence of oncogenic viruses. Thus, understanding this association may provide a relevant modification for developing personalized therapeutic options for treatment of NSCLC patients associated oncogenic viruses. Citation Format: Shaimaa Saeed, Amira Salah El-Din Youssef, Ahmed M. Fahmy, Nasra F. Abdel Fattah, Zeinab K. Hassan, Mohamed M. Hafez. Somatic EGFR mutations and oncogenic viruses in NSCLC Egyptian patients [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2025; Part 1 (Regular Abstracts); 2025 Apr 25-30; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2025;85(8_Suppl_1):Abstract nr 932.