title: Inactivation of the p15 gene in children with acute lymphoblastic leukemia.
abstract: BACKGROUND
  Tumor suppressor genes act on the control of cell cycle progression. In pediatric neoplasias, some of these genes may be considered to be markers for diagnosis or relapse, thus probably representing prognostic indicators.
  
  
  OBJECTIVE
  To study the inactivation of the p15 gene in children with acute lymphoblastic leukemia.
  
  
  METHODS
  Retrospective study.
  
  
  METHODS
  Laboratory of Molecular Biology, Department of Pediatrics, Faculdade de Medicina de Ribeiráo Preto, Universidade de São Paulo.
  
  
  METHODS
  Eighty-three children and adolescents with acute lymphoblastic leukemia were studied, with the examination of 83 bone marrow samples obtained at diagnosis, four obtained also during relapse, and two cerebrospinal fluid samples obtained from two cases of isolated relapse in the central nervous system.
  
  
  METHODS
  Homologous deletion of the p15 gene by multiplex polymerase chain reaction, and screening for point mutations by polymerase chain reaction/single-strand conformational polymorphism.
  
  
  RESULTS
  Deletion of exon 2 of the p15 gene was observed in 15 children, including one case in which deletion was only verified during isolated central nervous system relapse. No case of exon 1 deletion, or that was suggestive of point mutations, was observed and no association between p15 gene inactivation and classic risk factors was established.
  
  
  CONCLUSIONS
  According to the literature, inactivation of the p15 gene by deletion of exon 2 in acute lymphoblastic leukemia found in the population studied would be considered to be a molecular marker for diagnosis or relapse. However, no correlation between p15 gene deletion and clinical prognostic indicators was observed.
authors.affiliation: Department of Pediatrics, Faculdade de Medicina de Ribeiráo Preto, Universidade de São Paulo, Ribeiráo Preto, São Paulo, Brazil.
authors.forename: Rosana
authors.initials: R
authors.lastname: Cipolotti
authors.forename: José Alexandre Rodrigues
authors.initials: JA
authors.lastname: Lemos
authors.forename: Ricardo
authors.initials: R
authors.lastname: Defavery
authors.forename: Carlos Alberto
authors.initials: CA
authors.lastname: Scrideli
authors.forename: Amaury Lellis
authors.initials: AL
authors.lastname: Dal Fabbro
authors.forename: Luiz Gonzaga
authors.initials: LG
authors.lastname: Tone
mesh_terms: D018797:Cell Cycle Proteins / Q000235:genetics*; D002648:Child; D002675:Child, Preschool; D050762:Cyclin-Dependent Kinase Inhibitor p15; D019941:Cyclin-Dependent Kinase Inhibitor p16 / Q000235:genetics*; D005091:Exons / Q000235:genetics; D005260:Female; D017353:Gene Deletion; D020868:Gene Silencing; D016147:Genes, Tumor Suppressor; D005819:Genetic Markers; D006801:Humans; D007223:Infant; D008297:Male; D016133:Polymerase Chain Reaction; D018807:Polymorphism, Single-Stranded Conformational; D054198:Precursor Cell Lymphoblastic Leukemia-Lymphoma / Q000235:genetics*; D011379:Prognosis; D012189:Retrospective Studies; D025521:Tumor Suppressor Proteins
chemical_list: C493966:CDKN2B protein, human; D018797:Cell Cycle Proteins; D050762:Cyclin-Dependent Kinase Inhibitor p15; D019941:Cyclin-Dependent Kinase Inhibitor p16; D005819:Genetic Markers; D025521:Tumor Suppressor Proteins