title: The role of CDKN2A/B deletions in pediatric acute lymphoblastic leukemia.
abstract: The CDKN2A/B genes in the 9p21 chromosomal region are frequently involved in human cancer, including pediatric acute lymphoblastic leukemia (ALL). These genes encode 3 proteins that belong to the RB1 and TP53 pathways and act as tumor suppressors by regulating the G1/S checkpoint of the cell cycle. The prognostic value of deletions in the CDKN2A/B locus in ALL is controversial in part due to the limitations of the methodologies used. Further studies with advanced technologies are needed for elucidation. Future studies would also highlight whether CDK4/CDK6 selective inhibitors might be useful therapies for children with these genetic aberrations.
authors.affiliation: a Laboratory of Molecular Pediatric Hemato-Oncology , Institute of Medical and Molecular Genetics (INGEMM), Hospital Universitario La Paz , Madrid , Spain.
authors.forename: P
authors.initials: P
authors.lastname: Carrasco Salas
authors.affiliation: b Clinical Research Program , Cancer Research National Centre , Madrid , Spain.
authors.forename: L
authors.initials: L
authors.lastname: Fernández
authors.affiliation: c Innate Immune Research Group, IdiPAZ , Madrid , Spain.
authors.forename: M
authors.initials: M
authors.lastname: Vela
authors.affiliation: d Department of Pediatric Hemato-Oncology and Stem Cell Transplantation , Hospital Infantil Universitario La Paz , Madrid , Spain.
authors.forename: D
authors.initials: D
authors.lastname: Bueno
authors.affiliation: d Department of Pediatric Hemato-Oncology and Stem Cell Transplantation , Hospital Infantil Universitario La Paz , Madrid , Spain.
authors.forename: B
authors.initials: B
authors.lastname: González
authors.affiliation: c Innate Immune Research Group, IdiPAZ , Madrid , Spain.
authors.forename: J
authors.initials: J
authors.lastname: Valentín
authors.affiliation: a Laboratory of Molecular Pediatric Hemato-Oncology , Institute of Medical and Molecular Genetics (INGEMM), Hospital Universitario La Paz , Madrid , Spain.
authors.forename: P
authors.initials: P
authors.lastname: Lapunzina
authors.affiliation: a Laboratory of Molecular Pediatric Hemato-Oncology , Institute of Medical and Molecular Genetics (INGEMM), Hospital Universitario La Paz , Madrid , Spain.|c Innate Immune Research Group, IdiPAZ , Madrid , Spain.|d Department of Pediatric Hemato-Oncology and Stem Cell Transplantation , Hospital Infantil Universitario La Paz , Madrid , Spain.
authors.forename: A
authors.initials: A
authors.lastname: Pérez-Martínez
mesh_terms: D000293:Adolescent; D002648:Child; D002675:Child, Preschool; D002899:Chromosomes, Human, Pair 9 / Q000235:genetics / Q000378:metabolism; D050762:Cyclin-Dependent Kinase Inhibitor p15 / Q000235:genetics / Q000378:metabolism; D019941:Cyclin-Dependent Kinase Inhibitor p16; D050763:Cyclin-Dependent Kinase Inhibitor p18 / Q000235:genetics / Q000378:metabolism; D005260:Female; D059585:G1 Phase Cell Cycle Checkpoints / Q000187:drug effects / Q000235:genetics; D017353:Gene Deletion; D056426:Genetic Loci; D006801:Humans; D007223:Infant; D007231:Infant, Newborn; D008297:Male; D054198:Precursor Cell Lymphoblastic Leukemia-Lymphoma / Q000188:drug therapy / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D056286:Retinoblastoma Binding Proteins / Q000235:genetics / Q000378:metabolism; D059807:S Phase Cell Cycle Checkpoints / Q000187:drug effects / Q000235:genetics; D015398:Signal Transduction / Q000235:genetics; D016159:Tumor Suppressor Protein p53 / Q000235:genetics / Q000378:metabolism; D044767:Ubiquitin-Protein Ligases / Q000235:genetics / Q000378:metabolism
chemical_list: C000614131:CDKN2A protein, human; C493966:CDKN2B protein, human; D050762:Cyclin-Dependent Kinase Inhibitor p15; D019941:Cyclin-Dependent Kinase Inhibitor p16; D050763:Cyclin-Dependent Kinase Inhibitor p18; C000606393:RB1 protein, human; D056286:Retinoblastoma Binding Proteins; C495901:TP53 protein, human; D016159:Tumor Suppressor Protein p53; D044767:Ubiquitin-Protein Ligases
keywords: CDK4/CDK6 inhibitors; CDKN2A gene; CDKN2B gene; deletions; pediatric acute lymphoblastic leukemia; prognosis