Just Say No to ATOH: How HIC1 Methylation Might Predispose Medulloblastoma to Lineage Addiction

被引：21

作者：

Briggs, Kimberly J. ^{[2
]}

Eberhart, Charles G. ^{[2
,3
]}

Watkins, D. Neil ^{[1
,2
]}

机构：

[1] Monash Med Ctr, Monash Inst Med Res, Clayton, Vic 3168, Australia

[2] Johns Hopkins Univ, Sidney Kimmel Comprehens Canc Ctr, Baltimore, MD USA

[3] Johns Hopkins Univ, Sch Med, Dept Pathol, Baltimore, MD 21205 USA

来源：

CANCER RESEARCH | 2008年 / 68卷 / 21期

关键词：

D O I：

10.1158/0008-5472.CAN-08-1904

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Hypermethylated in cancer-1 (HICI) is a tumor suppressor frequently targeted for promoter hypermethylation in medulloblastoma, an embryonal tumor of the cerebellum. Recently, we showed that HICI is a direct transcriptional repressor of ATOH1, a proneural transcription factor required for normal cerebellar development, as well as for medulloblastoma cell viability. Because demethylating agents can induce reexpression of silenced tumor suppressors, restoring HICI function may present an attractive therapeutic avenue in medulloblastoma by exploiting an apparent addiction to ATOH1. [Cancer Res 2008;68(21):8654-6]

引用

页码：8654 / 8656

页数：3

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