title: Molecular cytogenetics of childhood acute myelogenous leukaemias.
abstract: Chromosome abnormalities of childhood acute myeloblastic leukaemia, observed at least in 70-80% of cases, are presently recognized as important parameters for diagnostic, prognostic and follow-up purposes. These abnormalities are numerical, structural or both numerical and structural. They are also classified in "primary" abnormalities, usually more or less related with one subtype of leukaemia, and "secondary" abnormalities thought to appear in a second time. Chromosome abnormalities of childhood acute myeloblastic leukaemia (AML) are not basically qualitatively different from those of adult AML. The main difference lies in the incidence of the various types of abnormalities, and these differences appear to be more marked for age extremes such as infants and elderly patients. In total, 3 common abnormalities are more frequently observed in childhood than in adult AML; t(8;21) in AML-M2, monosomy 7 in AML-M4, der(11q) in AML-M5. In addition, molecular rearrangements associated with chromosomal abnormalities are dependent on the type of rearrangement and not on age. As in adult AML, the prognostic value of chromosome abnormalities has been diversely evaluated; some anomalies seem to be related to a shorter survival than others independent of the various therapeutic protocols used. In the present work, chromosome abnormalities of childhood AML have been reviewed according to cytologic subtypes as well as to some clinical settings. Special attention has been paid to abnormalities frequently or exclusively encountered in children.
authors.affiliation: Hématologie Pédiatrique, Hôpital Saint-Louis, Paris, France.
authors.forename: T
authors.initials: T
authors.lastname: Leblanc
authors.forename: R
authors.initials: R
authors.lastname: Berger
mesh_terms: D018906:Antineoplastic Agents, Alkylating / Q000009:adverse effects; D002648:Child; D002675:Child, Preschool; D002869:Chromosome Aberrations / Q000235:genetics*; D025063:Chromosome Disorders; D002874:Chromosome Mapping; D050676:Core Binding Factor Alpha 2 Subunit; D004268:DNA-Binding Proteins / Q000235:genetics; D004314:Down Syndrome / Q000150:complications; D005796:Genes; D011495:Histone-Lysine N-Methyltransferase; D006801:Humans; D007223:Infant; D015470:Leukemia, Myeloid, Acute / Q000235:genetics*; D009006:Monosomy; D051788:Myeloid-Lymphoid Leukemia Protein; D009363:Neoplasm Proteins; D009687:Nuclear Proteins; D000071156:Promyelocytic Leukemia Protein; D011518:Proto-Oncogene Proteins; D011519:Proto-Oncogenes; D018168:Receptors, Retinoic Acid / Q000235:genetics; D014157:Transcription Factors / Q000235:genetics; D014178:Translocation, Genetic; D025521:Tumor Suppressor Proteins
chemical_list: D018906:Antineoplastic Agents, Alkylating; D050676:Core Binding Factor Alpha 2 Subunit; D004268:DNA-Binding Proteins; C497422:KMT2A protein, human; D009363:Neoplasm Proteins; D009687:Nuclear Proteins; D000071156:Promyelocytic Leukemia Protein; D011518:Proto-Oncogene Proteins; C493728:RUNX1 protein, human; D018168:Receptors, Retinoic Acid; D014157:Transcription Factors; D025521:Tumor Suppressor Proteins; C070576:PML protein, human; D051788:Myeloid-Lymphoid Leukemia Protein; D011495:Histone-Lysine N-Methyltransferase