Document Detail

Promoter hypermethylation profile of RASSF1A, FHIT, and sFRP1 in intracranial primitive neuroectodermal tumors.
MedLine Citation:
PMID:  16311119     Owner:  NLM     Status:  MEDLINE    
Medulloblastomas (MBs) and supratentorial primitive neuroectodermal tumors (SPNETs) are histologically alike intracranial PNETs found in different anatomical locations of the brain. Current evidence suggests that hypermethylation of promoter CpG islands is a common epigenetic event in a variety of human cancers. The aim of this study was to investigate whether promoter hypermethylation of putative tumor suppressor genes was involved in both types of intracranial PNETs. We examined the methylation status at promoter regions of RASSF1A, FHIT, and sFRP1 by methylation-specific polymerase chain reaction in a cohort of 25 primary MBs, 9 primary SPNETs, and 3 MB and 2 SPNET cell lines. Our results revealed no promoter hypermethylation of RASSF1A, FHIT, and sFRP1 in 2 normal cerebellar and 5 normal cerebral tissue specimens examined. In contrast, promoter hypermethylation of RASSF1A was detected in 100% of primary MBs, 67% (6/9) of primary SPNETs, and all PNET cell lines. The frequency of promoter hypermethylation of RASSF1A was significantly lower in SPNETs than in MBs (Fisher exact test, P = .014). Treatment of RASSF1A-deficient PNET cell lines with 5-aza-2'deoxycytidine, a demethylating agent, restored RASSF1A expression, providing evidence that promoter hypermethylation contributes to transcriptional silencing. In addition, promoter hypermethylation of FHIT and sFRP1 was detected in 22% (2/9) and 11% (1/9) of SPNETs, respectively, but not in any MBs studied. In conclusion, our study demonstrates that promoter hypermethylation of RASSF1A is a common event in intracranial PNETs, whereas FHIT and sFRP1 are epigenetically affected in a fraction of SPNETs.
Qing Chang; Jesse Chung-Sean Pang; Kay Ka Wai Li; Wai Sang Poon; Liangfu Zhou; Ho-Keung Ng
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Human pathology     Volume:  36     ISSN:  0046-8177     ISO Abbreviation:  Hum. Pathol.     Publication Date:  2005 Dec 
Date Detail:
Created Date:  2005-11-28     Completed Date:  2006-01-17     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  9421547     Medline TA:  Hum Pathol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1265-72     Citation Subset:  IM    
Department of Anatomical and Cellular Pathology, Prince of Wales Hospital, The Chinese University of Hong Kong, Hong Kong SAR, People's Republic of China.
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MeSH Terms
Acid Anhydride Hydrolases / genetics*,  metabolism
Brain Neoplasms / genetics*,  metabolism,  pathology
Cell Cycle Proteins / genetics*,  metabolism
Cell Line, Tumor
Child, Preschool
DNA Methylation*
DNA Primers / chemistry
DNA, Neoplasm / analysis
Neoplasm Proteins / genetics*,  metabolism
Neuroectodermal Tumors, Primitive / genetics*,  metabolism,  pathology
Protein-Serine-Threonine Kinases / genetics*,  metabolism
Reverse Transcriptase Polymerase Chain Reaction
Tumor Suppressor Proteins / genetics*,  metabolism
Reg. No./Substance:
0/Cell Cycle Proteins; 0/DNA Primers; 0/DNA, Neoplasm; 0/Neoplasm Proteins; 0/RASSF1 protein, human; 0/Tumor Suppressor Proteins; 0/fragile histidine triad protein; EC 2.7.1.-/ATR protein, human; EC Kinases; EC 3.6.-/Acid Anhydride Hydrolases

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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