Bioinformatics and Systems Medicine Laboratory
General information | Expression | Regulation | Mutation | Interaction

Basic Information

Gene ID

196528

Name

ARID2

Synonymous

BAF200|p200;AT rich interactive domain 2 (ARID, RFX-like);ARID2;AT rich interactive domain 2 (ARID, RFX-like)

Definition

ARID domain-containing protein 2|AT-rich interactive domain-containing protein 2|BRG1-associated factor 200|zinc finger protein with activation potential|zipzap|zipzap/p200

Position

12q12

Gene type

protein-coding

Source

Count: 2; Pubmed_search,Generif

Sentence

Abstract

ARID2: a new tumor suppressor gene in hepatocellular carcinoma.

Hepatocellular carcinoma (HCC) is one of the most common malignancies worldwide, however, genetic-environmental interactions and mechanisms associated with the development of HCC remains largely unclear. Our recent work described novel inactivating mutations of ARID2 (AT-rich interactive domain 2) in four major subtypes of HCC through exomic sequencing of ten HCV-associated HCCs and subsequent evaluation of the tumors from additional affected individuals. Here, we summarize the current knowledge about the relevance of ARID2 in HCC and the implication in future patient care.

"18.2% of individuals with HCV-associated HCC in the United States and Europe harbored ARID2 inactivation mutations, suggesting that ARID2 is a tumor suppressor gene that is relatively commonly mutated in this tumor subtype."

Through exomic sequencing of ten hepatitis C virus (HCV)-associated hepatocellular carcinomas (HCC) and subsequent evaluation of additional affected individuals, we discovered novel inactivating mutations of ARID2 in four major subtypes of HCC (HCV-associated HCC, hepatitis B virus (HBV)-associated HCC, alcohol-associated HCC and HCC with no known etiology). Notably, 18.2% of individuals with HCV-associated HCC in the United States and Europe harbored ARID2 inactivation mutations, suggesting that ARID2 is a tumor suppressor gene that is relatively commonly mutated in this tumor subtype.

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