Youwei Zhang1, Xiaobing Ye, Jian Geng, Longbang Chen. 1. Department of Medical Oncology, Jinling Hospital, Medical school of Nanjing University, Nanjing 210002, Jiangsu province, China.
Abstract
BACKGROUND/AIM: Deleted in Lung and Esophageal Cancer 1 (DLEC1) gene was a new candidate tumor suppressor gene, we evaluated the diagnostic role of DLEC1 methylation in gastric adenocarcinoma (GAC) and colorectal adenocarcinoma (CRAC). METHODOLOGY: Methylation-specific polymerase chain reaction (MSP) was used to determine the promoter methylation status of DLEC1 gene in tissue and serum DNA. DLEC1 gene expression was determined by immunohistochemistry. RESULTS: DLEC1 methylation was detected in 38.5% (25/65) of GAC and 45.1% (32/71) of CRAC tissues, while seldom in the adjacent normal tissues of stomach (8.0%, 4/50) and colorectum (7.1%, 4/56) (p < 0.001). The hypermethylation status of DLEC1 was associated with low or absent of DLEC1 protein expression both in tumor and pre-malignant lesions (p < 0.001), but not correlated with patients' clinicopathological features and elevated CEA/CA19-9 levels. Moreover, 33.8% (22/65) of GAC and 39.4% (28/71) of CRAC serums had DLEC1 methylation, which was higher than that in the serums of cancer-free controls (p < 0.001), and the concordance of DLEC1 methylation in tumor tissues and corresponding serum samples was well. CONCLUSION: Epigenetic inactivation of DLEC1 was crucial in gastric and colorectal carcinogenesis. DLEC1 methylation in serum may be a promise biomarker for GAC and CRAC early diagnosis.
BACKGROUND/AIM: Deleted in Lung and Esophageal Cancer 1 (DLEC1) gene was a new candidate tumor suppressor gene, we evaluated the diagnostic role of DLEC1 methylation in gastric adenocarcinoma (GAC) and colorectal adenocarcinoma (CRAC). METHODOLOGY: Methylation-specific polymerase chain reaction (MSP) was used to determine the promoter methylation status of DLEC1 gene in tissue and serum DNA. DLEC1 gene expression was determined by immunohistochemistry. RESULTS:DLEC1 methylation was detected in 38.5% (25/65) of GAC and 45.1% (32/71) of CRAC tissues, while seldom in the adjacent normal tissues of stomach (8.0%, 4/50) and colorectum (7.1%, 4/56) (p < 0.001). The hypermethylation status of DLEC1 was associated with low or absent of DLEC1 protein expression both in tumor and pre-malignant lesions (p < 0.001), but not correlated with patients' clinicopathological features and elevated CEA/CA19-9 levels. Moreover, 33.8% (22/65) of GAC and 39.4% (28/71) of CRAC serums had DLEC1 methylation, which was higher than that in the serums of cancer-free controls (p < 0.001), and the concordance of DLEC1 methylation in tumor tissues and corresponding serum samples was well. CONCLUSION: Epigenetic inactivation of DLEC1 was crucial in gastric and colorectal carcinogenesis. DLEC1 methylation in serum may be a promise biomarker for GAC and CRAC early diagnosis.