The aim of this study was to investigate the relationship between KRAS LCS6 mutation and endometrial cancer (EC). The study included 105 patients who had hysterectomy for benign reasons and 99 EC patients. The patients with Type 1 EC were classified according to histological properties, cancer stage, grade, tumour dimension, myometrial invasion (MMI), lymphovascular invasion (LVI), cytology, and number of positive lymph nodes. KRAS LCS6 mutation was examined in blood samples taken from all patients in both groups. No statistically significant difference was determined between the EC patients and the control group in demographic features. Weight and the Body Mass Index (BMI) values were higher in EC group (p <.001). While the incidence of this polymorphism is 5.8% throughout the world, the polymorphism rate was found to be 16.2% in the EC group and 12.4% in the control group, with no statistically significant difference determined (p >.05). Despite the higher rate of LCS6 polymorphism incidence in EC patients in this study conducted on a relatively large sample, there was not found to be a statistically significant difference in comparison with the control group. In addition, the presence of LCS6 polymorphism was not determined to have an effect on EC histopathological characteristics.Impact statementWhat is already known on this subject? Endometrial cancer (EC) is a genital system cancer which is one of the most widespread gynecological cancers seen in the USA and other developed countries, In EC, the most frequently seen gene mutations are PTEN tumour suppressor gene, KRAS, β1 catenin, BCL-2, CTNNB and P53 mutations. KRAS LCS6(let-7 miRNA binding region polymorphism) polymorphism has a worldwide incidence of 5.8% (Chin et al. 2008).There are studies shown that KRAS LCS6 polymorphism has an effect on developing EC (Lee et al. 2014), ovarian cancer(Ratner et al. 2010)and endometriosis in women (Grechukhina et al. 2012). What do the results of this study add? In our study, LCS6 located on KRAS 3’-UTR was found at the rate of 16.2% in Type 1 EC patients. This increase is noticeable when it is considered that the incidence of this polymorphism is 5.8% in the general population. The results of the current study supports the preliminary findings of Lee et al. What are the implications of these findings for clinical practice and/or further research? These new genetic markers could help to develop gene-targeted therapies, identify genetic basis of the disease and the factors that could affect the EC prognosis.