ReviewCancer research2008
Just say no to ATOH: how HIC1 methylation might predispose medulloblastoma to lineage addiction.
Review in Cancer research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
14 citing papers in PubMed, 21 citations in OpenAlex.
- Ferroptosis-related gene HIC1 in the prediction of the prognosis and immunotherapeutic efficacy with immunological activity.Frontiers in immunology · 2023Article
- Atonal bHLH transcription factor 1 is an important factor for maintaining the balance of cell proliferation and differentiation in tumorigenesis.Oncology letters · 2020Review
- Article
- ATOH1 Promotes Leptomeningeal Dissemination and Metastasis of Sonic Hedgehog Subgroup Medulloblastomas.Cancer research · 2017Article
- Prognostic relevance of high atonal homolog-1 expression in Merkel cell carcinoma.Journal of cancer research and clinical oncology · 2017Article
- The Role of Atonal Factors in Mechanosensory Cell Specification and Function.Molecular neurobiology · 2015Article
- Novel gene expression model for outcome prediction in paediatric medulloblastoma.Journal of molecular neuroscience : MN · 2013Article
- The genetics of hair cell development and regeneration.Annual review of neuroscience · 2013Review
- Deciphering HIC1 control pathways to reveal new avenues in cancer therapeutics.Expert opinion on therapeutic targets · 2013Review
- The role of Atonal transcription factors in the development of mechanosensitive cells.Seminars in cell & developmental biology · 2013Review
- Hypermethylated in cancer 1 (HIC1) recruits polycomb repressive complex 2 (PRC2) to a subset of its target genes through interaction with human polycomb-like (hPCL) proteins.The Journal of biological chemistry · 2012Article
- The receptor tyrosine kinase EphA2 is a direct target gene of hypermethylated in cancer 1 (HIC1).The Journal of biological chemistry · 2012Article
- Cerebellum development and medulloblastoma.Current topics in developmental biology · 2011Review
- Atoh1 inhibits neuronal differentiation and collaborates with Gli1 to generate medulloblastoma-initiating cells.Cancer research · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
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.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.