Epigenteic Alteration of DOK7 Gene CpG Island in Blood Leukocyte of Patients with Gastric Cancer and Intestinal Methaplasia

Document Type : Brief Report

Authors

1 Department of Medical Biotechnology, Medical Genetic group, National Institute of Genetic Engineering and Biotechnology, Tehran, Iran

2 Department of Radiation Oncology, Hamadan University of Medical Sciences, Mahdieh center, Hamadan, Iran

3 Department of Pathology, Hamadan University of Medical Sciences, Hamadan, Iran.

Abstract

Background: Intestinal metaplasia (IM) is a benign lesion with no serious concern for patients’ health. On the other 
hand, gastric cancer (GC) is a malignant lesion that has to be differentially diagnosed from benign intestinal metaplasia. 
Epigenetic modifications have been suggested to play an important role in cancer initiation and development, and they 
have been investigated as a reliable biomarker tool even for early cancer diagnosis. Whole blood leucocytes (WBC) are 
potentially the most accessible tissue for cancer early diagnosis, especially for GC, which is hard to diagnose in the early 
stage.
Objective: This study aims to investigate the methylation status of DOK7 gene CpG island in blood leukocytes of patients 
with IM and GC compared to normal control groups. 
Material and Method: DNA was extracted from the whole blood of 30 IM patients, 30 GC patients, and 34 normal 
controls samples, and MSRE-PCR was utilized to evaluate the loci methylation status.
Results: Significant hypermethylation of DOK7 gene CpG has been observed in GC 88.1 % (p < 0.001) and IM 66.0 % (p 
= 0.03) in comparison to the normal control group 56.8%. A cut‑off upper than 84.5 % of hypermethylation is considered 
as a presence of gastric cancer malignant lesions.
Conclusions: This is the first reported on hypermethylation in DOK7 CPG in blood leukocytes of patients with GC and 
IM and establishing a laboratory blood based test that may be useful as a novel biomarker test in the early diagnosis and 
screaning of GC and IM.

Keywords

Main Subjects


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