title: Epigenetic regulation of putative tumor suppressor TGFBI in human leukemias.
abstract: BACKGROUND
  Both in vitro and in vivo data have demonstrated the TGFBI gene functions as a putative tumor suppressor and is frequently downregulated in human tumors of different histological types. The hypermethylation of the TGFBI promoter, as one of the main regulatory mechanisms, is associated with TGFBI silencing. In this study, we used a methylation-specific PCR (MSP) method to evaluate the methylation status of the TGFBI promoter in human leukemias.
  
  
  METHODS
  Real-time RT-PCR and methylation-specific PCR approaches were performed to define the TGFBI expression and promoter methylation in human leukemia cell lines and clinical samples. Genomic DNA was isolated from peripheral blood mononuclear cells from leukemia patients, bisulfite-converted, and analyzed by the MSP method.
  
  
  RESULTS
  Hypermethylation of the TGFBI promoter occurred in leukemia cell lines and demethylation treatment reexpressed TGFBI at a substantially increased level in most of leukemia cell lines tested. Furthermore, a much higher level of CpG island methylation and a significantly lower TGFBI expression were also identified in clinical leukemia samples.
  
  
  CONCLUSIONS
  The results suggest an important role of promoter methylation in regulating TGFBI expression in leukemia, which provides a useful diagnostic marker for clinical management of human leukemias.
authors.affiliation: Center for Genome Variations and Precision Bio-Medicine, Beijing Institute of Genomics, Chinese Academy of Sciences, Beijing 100029, China.
authors.forename: Hongbo
authors.initials: H
authors.lastname: Fang
authors.affiliation: Center for Genome Variations and Precision Bio-Medicine, Beijing Institute of Genomics, University of Chinese Academy of Sciences, Beijing 100049, China.
authors.forename: Jing
authors.initials: J
authors.lastname: Liu
authors.affiliation: Center for Genome Variations and Precision Bio-Medicine, Beijing Institute of Genomics, Chinese Academy of Sciences, Beijing 100029, China.
authors.forename: Dan
authors.initials: D
authors.lastname: Guo
authors.affiliation: Department of Clinical Laboratory, First People's Hospital of Yueyang, Yueyang, Hunan 414000, China.
authors.forename: Peixiang
authors.initials: P
authors.lastname: Liu
authors.affiliation: Center for Genome Variations and Precision Bio-Medicine, Beijing Institute of Genomics, Chinese Academy of Sciences, Beijing 100029, China.
authors.forename: Yongliang
authors.initials: Y
authors.lastname: Zhao
mesh_terms: D045744:Cell Line, Tumor; D018899:CpG Islands / Q000235:genetics; D019175:DNA Methylation / Q000187:drug effects / Q000235:genetics; D044127:Epigenesis, Genetic / Q000187:drug effects / Q000235:genetics*; D016326:Extracellular Matrix Proteins / Q000235:genetics*; D006801:Humans; D007938:Leukemia / Q000453:epidemiology*; D011401:Promoter Regions, Genetic / Q000235:genetics; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013447:Sulfites / Q000494:pharmacology; D016212:Transforming Growth Factor beta / Q000235:genetics*; D000099222:betaIG-H3 Protein
chemical_list: D016326:Extracellular Matrix Proteins; D013447:Sulfites; D016212:Transforming Growth Factor beta; D000099222:betaIG-H3 Protein; C042345:hydrogen sulfite