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Differential E-cadherin Expression Patterns in Gastric Cancer and Their Potential Molecular Mechanisms

Author: JiangLiHong
Tutor: LiHong
School: Dalian Medical University
Course: Pathology and Pathophysiology
Keywords: gastric cancer E-cadherin transcriptional repressor Snail hypermethylation
CLC: R735.2
Type: Master's thesis
Year: 2006
Downloads: 74
Quote: 0
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Abstract


Background and ObjectiveGastric cancer (GC) is one of the commonest malignancies and the major cause of cancer-related deaths in China because of the later diagnosis and its strong tendency of local invasiveness and distal metastasis.Aberrant expressions of tumor-related genes are involved in carcinogenesis, e.g. downregulated and even diminished E-cadherin production. E-cadherin is a transmembrane homophilic glycoprotein that plays central roles in calcium-dependent adhesion of epithelial cells, the maintenance of cell differentiation and the normal architecture of epithelial tissues. It has been well documented that loss of E-cadherin protein serves as a biological indicator of cell dedifferentiation and patients’ poor prognosis.So far, the causes of E-cadherin downregulation have been still under investigation. Most reports about the status of E-cadherin in cancer cells are defined at protein level, and little attention has been paid to its mRNA level. Furthermore, no comprehensive investigation has been available concerning the relationship between E-cadherin transcription and translation in cancer cells. Our current study was therefore designed to figure out the above issues.It was found in this study that different patterns of E-cadherin transcription could be observed among the gastric cancer tissues checked, showing no change, more or less decrease in comparison to that revealed in relatively normal gastric mucosa. E-cadherin transcriptional repressor Snail and promoter hypermethylation were examined in this study to explain

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CLC: > Medicine, health > Oncology > Gastrointestinal Cancer > Gastric neoplasms
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