Epigenetic silencing of tumor suppressor genes (TSGs) by promoter CpG methylation and histone modification has been widely recognized as one of the major causes of tumorigenesis including hematological malignancies [1, 2]. Aberrant methylation of TSG is frequently detected even in the early stage of tumorigenesis, suggesting its potential as tumor biomarker for early detection and therapeutic targeting.
Deletions of the 3p22-21.3 region have been identified as one of the earliest molecular events in various malignancies , including naspharyngeal , head and neck , lung , gastric , breast , cervix  and renal  carcinomas, as well as lymphomas . A growing number of TSGs, including RASSF1A[12, 13], BLU/ZMYND10[14, 15], and CACNA2D2, have been identified in this region [17, 18]. Frequent inactivation of several 3p21.3 genes as functional TSGs, such as RASSF1 and BLU[14, 19], by promoter CpG methylation had been identified associated with tumor initiation and progression. For example, promoter methylation of RASSF1A has been shown related to poor prognosis and advanced tumor stage of certain tumor types [20–33]. Restoration of RASSF1A in cancer cell lines inhibited tumor cell growth and metastasis . Thus, 3p22-21.3 is a critical TSG cluster in tumorigenesis [3, 18].
Deleted in lung and esophageal cancer 1 (DLEC1), a 3p22 cluster genes, was first identified as a TSG in esophageal and lung cancers . Downregulation of DLEC1 by promoter methylation has been found in multiple cancers, including nasopharyngeal [36, 37], ovarian , lung , hepatocellular , gastric , renal , and breast carcinomas , suggesting its potential as a broad TSG [44, 45]. Remarkably, DLEC1 was methylated in breast cancer as well as pre-invasive lesions but rarely in normal breast tissues, indicating its potential as an epigenetic marker for early tumors .
In this study, we examined the expression and methylation status of DLEC1 in lymphoma cell lines and tissues, and evaluated its potential as a tumor marker for the early detection of hematologic tumors.