title: Genomic and allelic expression status of the p73 gene in human neuroblastoma.
abstract: METHODS
  The p53 gene homologue, p73, is located on the 1p36-3 locus, which is frequently deleted in human neuroblastoma (NB). A survey of 61 NB showed that among 33% of informative cases, p73 loss of heterozygosity (LOH) occurred in 7 of 20 (35%).
  
  
  RESULTS
  LOH pattern of vicinal markers suggested that the p73 gene could not be considered as the candidate NB suppressor gene. Moreover, comparative measurements of allelic expression in tumors and corresponding patient lymphocytes indicate that pure biallelism is much more frequent in lymphocytes than in tumors (71% vs 30%, P= 0.05), which suggests that disequilibrated allelic expression is associated with NB disease.
  
  
  CONCLUSIONS
  Therefore, in the p73 LOH NBs, the p73 gene could be altered in the maintained allele not by mutations [Ishimiya et al.: Med Pediatr Oncol, this issue], but rather by an abnormal transcription.
authors.affiliation: Department of Clinical Biology, Institut Gustave Roussy, Villejuif, France.
authors.forename: M
authors.initials: M
authors.lastname: Barrois
authors.forename: M K
authors.initials: MK
authors.lastname: Eychenne
authors.forename: M J
authors.initials: MJ
authors.lastname: Terrier-Lacombe
authors.forename: N
authors.initials: N
authors.lastname: Duarte
authors.forename: C
authors.initials: C
authors.lastname: Dubourg
authors.forename: S
authors.initials: S
authors.lastname: Douc-Rasy
authors.forename: A
authors.initials: A
authors.lastname: Chompret
authors.forename: M
authors.initials: M
authors.lastname: Khagad
authors.forename: O
authors.initials: O
authors.lastname: Hartmann
authors.forename: D
authors.initials: D
authors.lastname: Caput
authors.forename: J
authors.initials: J
authors.lastname: Bénard
mesh_terms: D000483:Alleles; D002878:Chromosomes, Human, Pair 1 / Q000235:genetics* / Q000648:ultrastructure; D018076:DNA, Complementary / Q000235:genetics; D004268:DNA-Binding Proteins / Q000096:biosynthesis / Q000235:genetics*; D015972:Gene Expression Regulation, Neoplastic; D016147:Genes, Tumor Suppressor; D006801:Humans; D019656:Loss of Heterozygosity; D008214:Lymphocytes / Q000378:metabolism / Q000648:ultrastructure; D009363:Neoplasm Proteins / Q000096:biosynthesis / Q000235:genetics*; D014411:Neoplastic Stem Cells / Q000378:metabolism / Q000648:ultrastructure; D009447:Neuroblastoma / Q000235:genetics*; D009687:Nuclear Proteins / Q000096:biosynthesis / Q000235:genetics*; D020033:Protein Isoforms / Q000096:biosynthesis / Q000235:genetics; D012333:RNA, Messenger / Q000096:biosynthesis; D012334:RNA, Neoplasm / Q000096:biosynthesis; D020133:Reverse Transcriptase Polymerase Chain Reaction; D000072160:Tumor Protein p73; D025521:Tumor Suppressor Proteins
chemical_list: D018076:DNA, Complementary; D004268:DNA-Binding Proteins; D009363:Neoplasm Proteins; D009687:Nuclear Proteins; D020033:Protein Isoforms; D012333:RNA, Messenger; D012334:RNA, Neoplasm; C000606460:TP73 protein, human; D000072160:Tumor Protein p73; D025521:Tumor Suppressor Proteins