Just say no to ATOH: How HIC1 methylation might predispose medulloblastoma to lineage addiction

Kimberly J. Briggs, Charles G. Eberhart, D. Neil Watkins

Research output: Contribution to journalReview article

Abstract

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.

Original languageEnglish (US)
Pages (from-to)8654-8656
Number of pages3
JournalCancer Research
Volume68
Issue number21
DOIs
StatePublished - Nov 1 2008

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

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