Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2009 Dec;195(2):112-9.
doi: 10.1016/j.cancergencyto.2009.06.021.

Methylation profiling of tumor suppressor genes and oncogenes in hepatitis virus-related hepatocellular carcinoma in northern India

Manjula Kiran  1 , Yogesh K Chawla, Jyotdeep Kaur
Affiliations

Methylation profiling of tumor suppressor genes and oncogenes in hepatitis virus-related hepatocellular carcinoma in northern India

Manjula Kiran et al. Cancer Genet Cytogenet. 2009 Dec.

Abstract

Hepatocellular carcinoma (HCC) is the fifth most common cancer in India, and hepatitis B virus and hepatitis C virus infections are major risk factors. DNA methylation alterations have been linked to various carcinomas in different populations. Aberrant CpG island methylation of genes has been recognized in HCC, information is limited for hepatitis virus-related hepatocarcinogenesis. HCC risk has not previously been associated with gene-specific DNA methylation in India. Promoter region methylation of a panel of six tumor suppressor genes (CDKN2A, CDKN2B, CDH1, GSTP1, SOCS1, and APC) and three oncogenes (MYC, HRAS, and KRAS) was determined by methylation-specific PCR among 23 HCC samples and 20 control hepatitis samples. CDKN2B methylation frequency in HCC was double that for hepatitis, and methylation allele density of APC, GSTP1, and CDKN2B increased 2.2-, 2.3-, and 7.6-fold, respectively. Epigenetic silencing of tumor suppressor genes starts during viral infection and progresses toward HCC with the chronicity of the disease. Findings of altered methylation status support involvement of these tumor suppressor genes in HCC. MYC showed decreased methylation in HCC, relative to hepatitis. These observations on DNA methylation suggest the involvement of CDKN2B, SOCS1, CDH1, GSTP1, and MYC in pathogenesis of HCC in India and implicate altered DNA methylation in the molecular pathogenesis.

PubMed Disclaimer

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

Publication types