Balkan Journal of Medical Genetics

THE FREQUENCY OF EGFR AND KRAS MUTATIONS IN THE TURKISH POPULATION WITH NON-SMALL CELL LUNG CANCER AND THEIR RESPONSE TO ERLOTINIB THERAPY
Demiray A, Yaren A, Karagenç N, Bir F, Demiray AG, Karagür ER, Tokgün O, Elmas L, Akça H, https://orcid.org/0000-0002-3343-0184.
*Corresponding Author: Professor Dr. Hakan Akça, Cancer Research Center, Pamukkale University, 11 University Street, Denizli Turkey. E-mail: hakca@pau.edu.tr (primary), hakanakca@yahoo.com
page: 21

INTRODUCTION

Lung cancer is one of the main leading causes of cancer death, and the most common cancer after prostate and breast cancers, in respect to prevalence [1]. The 5-year overall survival is 15.0% in patients with non-small cell lung cancer (NSCLC) [1]. Overall survival rates increase with surgical, chemotherapy and radiotherapy treatments in early stages of the cancer [2]. Recently, immunotherapy and molecular targeted therapy have been used to treat cancer patients. Erlotinib and gefitinib, which are the inhibitors of epidermal growth factor receptor (EGFR) tyrosine kinases are molecular targeted agents. These agents have been used to inhibit certain EGFR tyrosine kinase mutations. Both of them can pass through the phospholipid membrane into the cell, and these agents compete with adenosine triphosphate (ATP) to bind the ATP binding pocket of EGFR. The EGFR, a transmembrane glycoprotein of 170 kDa consisting 1186 amino acids, is localized in the 7q12 chromosome region. It is known that the EGFR receptor has mutations in the tyrosine kinase region of 18-21 exons in NSCLC cells and correlate therapy response. These EGFR mutations are more common in Asian, Caucasian and non smoking women [4]. K-ras, a downstream protein, becomes constantly active as a result of EGFR auto-phosphorylation. The Kirsten ras sarcoma (KRAS) gene belongs to Ras gene family and homolog of Kristen rat sarcoma viral oncogene [5-8]. It is localized at the chromosome 12 (12q12.1) region and consists of six exons transcribed as a small guanosine triphosphatease (GTPase) consists of 21k Da and 189 amino acids [5,7]. Codons 12 and 13 have GTPase-acting proteins (GTPs) binding site in the KRAS gene. Codon 61 is the switch II region that regulates Ras protein. Mutations at codons 12, 13 and 61 prevent GTP hydrolysis causing K-ras protein constantly active situation. Studies have shown that NSCLC patients with KRAS mutations have lower survival rates than those without KRAS mutations [6]. In our study, we investigated the frequency of EGFR and KRAS mutations and effects of anti-EGFR tyrosine kinase inhibitors treatment in Turkish NSCLC patients. This is the first large-scale study that investigates EGFR and KRAS mutations in 300 patients with NSCLC in Turkey.

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