Please use this identifier to cite or link to this item:
Title: CRH-BP as a possible diagnostic marker for Hepatocellular carcinoma
Keywords: Corticotrophin-releasing hormone binding protein, Methylation, Hepatocellular carcinoma, microarray,
Issue Date: 15-Sep-2007
Citation: GAYATHRI D/O MOHANAKRISHNAN (2007-09-15). CRH-BP as a possible diagnostic marker for Hepatocellular carcinoma. ScholarBank@NUS Repository.
Abstract: Hepatocellular Carcinoma (HCC) is especially prevalent in parts of Asia and Africa. About 80% of people with hepatocellular carcinomas have cirrhosis. Chronic infection with the hepatitis B virus and hepatitis C virus also increases the risk of developing hepatocellular carcinoma. HCC is a difficult cancer to diagnose and thus treatment is usually administered too late. A previous microarray study done revealed 218 genes with potential to be diagnostic markers due to significant differential expression in tumour relative to non-tumor tissues. Corticotrophin-releasing hormone binding protein (CRH-BP) was one of these genes. It is a secreted protein that is associated with regulation of CRH. CRH-BP expression was down-regulated in HCC derived cell lines and clinical samples as measured by quantitative real-time PCR and regular RT-PCR. To explore the possible reason behind this down-regulation, MSP and 5-Aza-dC treatment was carried out. These two procedures confirmed that CpG island hypermethylation was the cause of the gene silencing in HCC. Over-expression of CRH-BP in HCC cell lines did not affect cell proliferation in liquid culture and anchorage- independent growth in soft agar. We thus successfully demonstrated that CRH-BP was a gene silenced in HCC due to CpG island hypermethylation and may have potential to be a diagnostic marker for HCC.
Appears in Collections:Master's Theses (Open)

Show full item record
Files in This Item:
File Description SizeFormatAccess SettingsVersion 
Gayathri Mohanakrishnan.pdf4.83 MBAdobe PDF



Page view(s)

checked on Apr 20, 2019


checked on Apr 20, 2019

Google ScholarTM


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.