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

¹ The Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University and ² Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland; and ³ Monash Institute of Medical Research, Monash Medical Centre, Australia

Requests for reprints: D. Neil Watkins, Monash Institute of Medical Research Monash Medical Centre, 246 Clayton Road, Clayton Vic 3168 Australia. Phone: 613-9594-7165; Fax: 613-9594-7167; E-mail: neil.watkins{at}med.monash.edu.au.

Key Words: HIC1 • PTCH • ATOH1 • Math1 • medulloblastoma

Hypermethylated in cancer-1 (HIC1) is a tumor suppressor frequently targeted for promoter hypermethylation in medulloblastoma, an embryonal tumor of the cerebellum. Recently, we showed that HIC1 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 HIC1 function may present an attractive therapeutic avenue in medulloblastoma by exploiting an apparent addiction to ATOH1. [Cancer Res 2008;68(21):8654–6]