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Gastric cancer is one of the most frequently diagnosed cancers worldwide [1]. In 2020, it is estimated that there will be more than 27,000 new cases and more than 11,000 patients will die from the disease, in the United States [2]. A global epigenetic marker is methylation of specific DNA bases. Several genes are generally hypomethylated in cancer patients, whereas tumor suppressor genes are hypermethylated in the vast majority of cases [3]. One of the most important events in carcinogenesis is the hypermethylation of CpG islands of the promoter region of these genes [4]. This procedure may affect the function of the aforementioned genes, involved in critical cell functions, such as DNA repair, cell cycle regulation, metabolism, cell–cell interactions, angiogenesis, apoptosis etc., leading to cancer development [5]. Methylation of the promoter region of tumor suppressor genes leads to inactivation of them, whereas unmethylated promoters are considered active, so the methylation patterns of cancer cells is translated into gene expression patterns. Cell-free DNA methylation may be used for the detection of treatment resistance in cancer patients. This resistance can be due to the reversal of existent or novel DNA changes induced by drugs. In many studies, DNA methylation patterns have been evaluated as predictors of treatment response in cancer patients, including breast and colon cancer patients. The relapse of the disease after chemotherapy is likely to be due, to some extent, to changes in the methylation pattern of DNA, which are induced by chemotherapy itself. On the other hand, the relapse of the disease may be due to methylation patterns already present in the tumor before the onset of any treatment, so that specific methylation patterns cause a more aggressive phenotype with a poor response to chemotherapy [6]. SOX17 has a very important role in regulating the growth and function of progenitor cells located in bone marrow via suppression of the activation of wnt signaling pathway. It seems thatmethylation of this gene results in activation of the wnt signaling pathway [7]. RASSF1A gene is responsible for the production of RASSF1A protein which is involved in the regulation of microtubules, the maintenance of genomic stability, the modification of apoptosis, the mobility of cells, the regulation of cell cycle and the control of tumor infiltration [8, 9]. Wif-1 gene (wnt inhibitory factor-1) acts as an antagonist of the wnt signaling pathway and is frequently methylated in many cancer patients [10]. In *Corresponding author: Evangelos Karamitrousis, Department of Oncology, Medical School, Democritus University of Thrace, Alexandroupolis, Greece, E-mail: vkaramitrousis@gmail.com Ioanna Balgkouranidou, Nikolaos Xenidis, Kyriakos Amarantidis, Eirini Biziota, Triantafyllia Koukaki and Stylianos Kakolyris, Department of Oncology, Medical School, Democritus University of Thrace, Alexandroupolis, Greece Gregorios Trypsianis, Department of Medical Statistics, Medical School, Democritus University of Thrace, Alexandroupolis, Greece Anastasios Karayiannakis and Heleni Bolanaki, Second Department of Surgery, Medical School, Democritus University of Thrace, Alexandroupolis, Greece Ekaterini Chatzaki and Georgios Kolios, Laboratory of Pharmacology, Medical School, Democritus University of Thrace, Alexandroupolis, Greece Evi Lianidou, Analysis of Circulating Tumor Cells, Laboratory of Analytical Chemistry, Department of Chemistry, University of Athens, Athens, Greece Maria Lambropoulou, Laboratory of Histology-Embryology, Medical School, Democritus University of Thrace, Alexandroupolis, Greece Clin Chem Lab Med 2021; 59(2): e73–e75

Association between SOX17 , Wif -1 and RASSF1A promoter methylation status and response to chemotherapy in patients with metastatic gastric cancer