EGFR and KRAS Oncogene Expressions Among Lung Cancer Patients in North Sumatera

Background: The urge in molecular alterations in cancer study showed new directions of lung cancer therapy to targeted therapy era. Nevertheless, there was a surge of resistance in targeted therapy due to double mutations in the oncogenic driver and the acquired resistance in T790M in EGFR. Unfortunately, there was still data limitations in epidemiological data in the expressions of EGFR and KRAS in Indonesia, particularly North Sumatera. Aims: The aim of this study was to determine the clinical characteristics of KRAS dan EGFR mutations in lung cancer patients in North Sumatera and whether there was an association between KRAS mutations and the therapy response of patients with and without EGFR-TKI. Methods: This is an observational study with retrospective cohort enrolled subjects diagnosed with lung cancer confirmed by histopathology examinations. EGFR and KRAS mutations were detected using sanger sequencing from the extractions of paraffin block using certain primers particularly in exon 2 of KRAS, exon 19, and exon 21 of EGFR. Therapy response was measured by RECIST criteria after 3 months of chemotherapy and targeted therapy. Results: Total 52 subjects had involved and completed all study procedure. There was none of exon 2 KRAS mutations and 6 subjects had EGFR mutations composed by 3 subjects had single mutations of exon 19, 1 subject had intron 190 mutations, and 2 subjects had double mutations. After 3 months of therapy, RECIST criteria was performed and showed no associations between EGFR mutations and RECIST with p-value: 0.08. Conclusions: KRAS mutations was not the cause of resistance in both systemic chemotherapy and EGFR-TKI in North Sumatera Populations.