Oncotarget

Research Papers:

Telomerase reverse transcriptase promoter mutations in hepatitis B virus-associated hepatocellular carcinoma

Xunjun Yang _, Xiuchan Guo, Yao Chen, Guorong Chen, Yin Ma, Kate Huang, Yuning Zhang, Qiongya Zhao, Cheryl A. Winkler, Ping An and Jianxin Lyu

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Oncotarget. 2016; 7:27838-27847. https://doi.org/10.18632/oncotarget.8539

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Abstract

Xunjun Yang1,2, Xiuchan Guo1,3, Yao Chen4, Guorong Chen4, Yin Ma1, Kate Huang4, Yuning Zhang1, Qiongya Zhao1, Cheryl A. Winkler5, Ping An5, Jianxin Lyu1

1Key Laboratory of Laboratory Medicine, Ministry of Education, Zhejiang Provincial Key Laboratory of Medical Genetics, Wenzhou Medical University, Wenzhou, Zhejiang, China

2Department of Laboratory Medicine, The Second Affiliated Hospital & Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, China

3ICF International, Atlanta, GA, USA

4Department of Pathology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, China

5Basic Research Laboratory, Center for Cancer Research, National Cancer Institute, Leidos Biomedical Research, Inc., Frederick National Laboratory for Cancer Research, Frederick, MD, USA

Correspondence to:

Ping An, email: [email protected]

Jianxin Lyu, email: [email protected]

Keywords: hepatocellular carcinoma, TERT, mutation, telomerase reverse transcriptase

Received: February 01, 2016     Accepted: March 28, 2016     Published: April 1, 2016

ABSTRACT

Telomerase reverse transcriptase (TERT) promoter mutations are among the most frequent noncoding somatic mutations in multiple cancers, including hepatocellular carcinoma (HCC). The clinical and pathological implications of TERT promoter mutations in hepatitis B virus (HBV)-associated HCC have not been resolved. To investigate TERT promoter mutations, protein expression, and their clinical-pathological implications, we sequenced the TERT promoter region for hotspot mutations in HCC tissues and performed immunostaining for TERT protein expression from HBV-associated HCC in Chinese patients. Of 276 HCC tumor DNA samples sequenced, 85 (31%) carried TERT promoter mutations. TERT promoter mutations were more frequent in those with low α-fetoprotein (AFP) serum levels (p = 0.03), advanced age (p = 0.04), and in those lacking HCC family history (p = 0.02), but were not correlated with HCC stages and grades. TERT protein levels were higher in HCC (n = 28) compared to normal liver tissues (n = 8) (p =0.001), but did not differ between mutated and non-mutated tumor tissues. In conclusion, TERT promoter mutations are common somatic mutations in HCC of Han Chinese with HBV infection. Detection of TERT promoter mutations in those with low levels of AFP may aid diagnosis of HCC with atypical presentation.


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