title: Human polyomavirus BK (BKV) and neuroblastoma: mechanisms of oncogenic action and possible strategy for novel treatment.
abstract: BACKGROUND
  We reported previously that nearly all human neuroblastomas analyzed contain and express genomic DNA sequences deriving from the human polyomavirus BK (BKV) [Flaegstad et al.: Cancer Res 59:1160-1163, 1999].
  
  
  METHODS
  Here we show that the BKV large T antigen is expressed and bound to p53 in neuroblastoma cells and that this interference compromises the tumor suppressor function of p53.
  
  
  RESULTS
  Treatment of neuroblastoma cells with large T antigen antisense constructs relocated active p53 to the nucleus. The relocation event was accompanied by enhanced p21(waf1/cip1) expression as well as induced apoptosis.
  
  
  CONCLUSIONS
  Continuous antisense oligonucleotide treatment of nude rats with human neuroblastoma xenografts resulted in a significant but incomplete reduction of tumor growth compared to rats treated with saline.
authors: Department of Pediatrics, Faculty of Medicine, University of Tromsø, Norway.
authors: G E
authors: GE
authors: Jørgensen
authors: J I
authors: JI
authors: Johnsen
authors: F
authors: F
authors: Ponthan
authors: P
authors: P
authors: Kogner
authors: T
authors: T
authors: Flaegstad
authors: T
authors: T
authors: Traavik
mesh_terms: D000818:Animals; D000952:Antigens, Polyomavirus Transforming / Q000032:analysis* / Q000276:immunology*; D016158:Genes, p53 / Q000276:immunology*; D006801:Humans; D009447:Neuroblastoma / Q000235:genetics* / Q000628:therapy / Q000821:virology*; D051381:Rats; D014407:Tumor Cells, Cultured
chemical_list: D000952:Antigens, Polyomavirus Transforming