Abstract
BackgroundDEK, as an oncoprotein, plays an important role in cancer development and progression. This study aimed to investigate the clinicopathological significance of DEK overexpression in patients with gastric cancer.Materials and methodsThe expression of DEK protein was evaluated by immunohistochemical (IHC) staining of 172 gastric cancer samples with complete clinicopathological features, and the correlation between DEK expression and clinicopathological features was examined. Survival rates were also calculated using the Kaplan-Meier method in gastric cancer patients with complete survival data.ResultsDEK protein showed a strictly nuclear staining pattern in gastric cancers with IHC and immunofluorescence. The strongly positive rate of DEK protein was 60.5% (104/172) in gastric cancers, which was significantly higher than that in either gastric dysplasia (19.4%, 7/36) or adjacent normal mucosa (0%, 0/27). DEK expression in gastric cancer correlated to tumor size, differentiation, clinical stage, disease-free survival, and overall survival rates. Further analysis showed that patients with early-stage gastric cancer and high DEK expression had shorter disease-free survival and overall survival duration than those with low DEK expression.ConclusionHigh level of DEK protein expression predicts the poor prognosis of patients with gastric cancer. DEK expression might be potentially used as an independent effective biomarker for prognostic evaluation of gastric cancers.Virtual slidesThe virtual slide(s) for this article can be found here: http://www.diagnosticpathology.diagnomx.eu/vs/5050145571193097
Highlights
Gastric cancer is one of the most common cancers worldwide, and it is the second most common cause of cancer death [1]
High level of DEK protein expression predicts the poor prognosis of patients with gastric cancer
DEK expression might be potentially used as an independent effective biomarker for prognostic evaluation of gastric cancers
Summary
Gastric cancer is one of the most common cancers worldwide, and it is the second most common cause of cancer death [1]. Human DEK was initially demonstrated to be the target of a recurrent t(6;9) translocation that generates fusion with CAN in a subset of acute myeloid leukemia (AML) patients [6]. It was identified as an oncoprotein and has a molecular weight of 42Kda. DEK plays an important role in cell processes and participates in a variety of cellular metabolic functions, such as global heterochromatin integrity [7], transcriptional control [8], mRNA splicing [9], DNA replication [10], DNA damage repair and susceptibility [11]. This study aimed to investigate the clinicopathological significance of DEK overexpression in patients with gastric cancer
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