Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1995-4-7
pubmed:abstractText
Since in AML differentiation is abnormal but not absent, a hierarchy of stem cells, progenitor cells and more differentiated cells is postulated. The leukemic stem cell might also be characterized by the expression of CD34 and the absence of differentiation markers. Bone marrow samples of 33 AML patients, including 10 patients both at presentation and after relapse, were double labeled for CD34 and CD33. In 14/33 AML less than 1% of the labeled cells were found in the CD34+/33- fraction. After relapse a certain shift towards a more primitive phenotype was observed, but in 4/5 relapsed AML the CD34+/33- fraction remained below 1%. Single cells from the different subfractions were cultured and showed heterogeneous cluster and colony growth in both the CD34-/33+ and CD34+/33+ fraction. More colonies were observed in the CD34+/33- fraction. In AML with a more 'mature' phenotype (low number of CD34+/CD33- cells), highly proliferative myeloid, erythroid and mixed colonies could be cloned exclusively from this small CD34+/33- fraction. In five patients with numerical chromosomal abnormalities all these highly proliferative colonies appeared disomic using in situ hybridization (ISH) with centromeric probes. Based on these data we conclude that the CD34+/33- cell fraction in AML with a more mature immunophenotype (small fraction of cells CD34+/33-) comprise residual normal progenitors, while no primitive leukemic progenitors could be identified.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0887-6924
pubmed:author
pubmed:issnType
Print
pubmed:volume
9
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
450-7
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
1995
pubmed:articleTitle
Residual normal, highly proliferative progenitors can be isolated from the CD34+/33- fraction of AML with a more differentiated phenotype (CD33+).
pubmed:affiliation
Department of Medicine, University Hospital Nijmegen, The Netherlands.
pubmed:publicationType
Journal Article, Comparative Study