Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2011-6-22
pubmed:abstractText
Leukaemia is often associated with genetic alterations such as translocations, amplifications and deletions, and recurrent chromosome abnormalities are used as markers of diagnostic and prognostic relevance. However, a proportion of acute myeloid leukaemia (AML) cases have an apparently normal karyotype despite comprehensive cytogenetic analysis. Based on conventional cytogenetic analysis of banded chromosomes, we selected a series of 23 paediatric patients with acute myeloid leukaemia and performed whole genome array comparative genome hybridization (aCGH) using DNA samples derived from the same patients. Imbalances involving large chromosomal regions or entire chromosomes were detected by aCGH in seven of the patients studied. Results were validated by fluorescence in situ hybridization (FISH) to both interphase nuclei and metaphase chromosomes using appropriate bacterial artificial chromosome (BAC) probes. The majority of these copy number alterations (CNAs) were confirmed by FISH and found to localize to the interphase rather than metaphase nuclei. Furthermore, the proliferative states of the cells analyzed by FISH were tested by immunofluorescence using an antibody against the proliferation marker pKi67. Interestingly, these experiments showed that, in the vast majority of cases, the changes appeared to be confined to interphase nuclei in a non-proliferative status.
pubmed:grant
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/21694761-10572083, http://linkedlifedata.com/resource/pubmed/commentcorrection/21694761-11110676, http://linkedlifedata.com/resource/pubmed/commentcorrection/21694761-11355922, http://linkedlifedata.com/resource/pubmed/commentcorrection/21694761-11901514, http://linkedlifedata.com/resource/pubmed/commentcorrection/21694761-11951177, http://linkedlifedata.com/resource/pubmed/commentcorrection/21694761-12393388, http://linkedlifedata.com/resource/pubmed/commentcorrection/21694761-12393746, http://linkedlifedata.com/resource/pubmed/commentcorrection/21694761-14726504, http://linkedlifedata.com/resource/pubmed/commentcorrection/21694761-15010150, http://linkedlifedata.com/resource/pubmed/commentcorrection/21694761-15870172, http://linkedlifedata.com/resource/pubmed/commentcorrection/21694761-15961730, http://linkedlifedata.com/resource/pubmed/commentcorrection/21694761-16010415, http://linkedlifedata.com/resource/pubmed/commentcorrection/21694761-16418595, http://linkedlifedata.com/resource/pubmed/commentcorrection/21694761-16455956, http://linkedlifedata.com/resource/pubmed/commentcorrection/21694761-16498392, http://linkedlifedata.com/resource/pubmed/commentcorrection/21694761-16864856, http://linkedlifedata.com/resource/pubmed/commentcorrection/21694761-17015806, http://linkedlifedata.com/resource/pubmed/commentcorrection/21694761-17268525, http://linkedlifedata.com/resource/pubmed/commentcorrection/21694761-17384204, http://linkedlifedata.com/resource/pubmed/commentcorrection/21694761-17488484, http://linkedlifedata.com/resource/pubmed/commentcorrection/21694761-18162393, http://linkedlifedata.com/resource/pubmed/commentcorrection/21694761-19651600, http://linkedlifedata.com/resource/pubmed/commentcorrection/21694761-19880497, http://linkedlifedata.com/resource/pubmed/commentcorrection/21694761-20001230, http://linkedlifedata.com/resource/pubmed/commentcorrection/21694761-8174084, http://linkedlifedata.com/resource/pubmed/commentcorrection/21694761-8799815, http://linkedlifedata.com/resource/pubmed/commentcorrection/21694761-9510506, http://linkedlifedata.com/resource/pubmed/commentcorrection/21694761-9746770
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:status
MEDLINE
pubmed:issn
1932-6203
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
6
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
e20607
pubmed:meshHeading
pubmed:year
2011
pubmed:articleTitle
Genomic imbalances are confined to non-proliferating cells in paediatric patients with acute myeloid leukaemia and a normal or incomplete karyotype.
pubmed:affiliation
Centre for Cell and Chromosome Biology and Brunel Institute of Cancer Genetics and Pharmacogenomics, Division of Biosciences, Brunel University, West London, United Kingdom.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't