Linked Life Data

9927191

Source:http://linkedlifedata.com/resource/pubmed/id/9927191

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1999-2-16
pubmed:abstractText
The mechanism leading to the expanding population of maturing myeloid cells which characterises chronic myeloid leukemia (CML) remains obscure. Because of its ability to mimic the proliferative and cell survival functions of hematopoietic growth factors, we hypothesized that the oncogene activated in CML, BCR-ABL, might also influence differentiation. To test this hypothesis, we examined the effects of expressing BCR-ABL on the myeloid differentiation of murine M1 leukemic cells, which cease dividing and differentiate into macrophages in the presence of the cytokines leukemia inhibitory factor (LIF) or interleukin (IL)-6. We found that BCR-ABL induced macrophage differentiation in M1 cells, accompanied by increased expression of macrophage cell surface markers and the acquisition of phagocytic ability. interestingly, clones of M1 cells which expressed BCR-ABL remained in cell cycle and were refractory to the growth inhibition and apoptosis induced by IL-6 or LIF in parental M1 cells. These cells also expressed inappropriately high levels of c-MYC mRNA for their degree of differentiation, which may have been important in maintaining cellular proliferation. These data suggest that BCR-ABL can stimulate both differentiation and proliferation and that these characteristics may contribute to the phenotype observed in CML.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0950-9232
pubmed:author
pubmed:issnType
Print
pubmed:day
14
pubmed:volume
18
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
343-52
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed-meshheading:9927191-Animals, pubmed-meshheading:9927191-Cell Cycle, pubmed-meshheading:9927191-Cell Differentiation, pubmed-meshheading:9927191-Cell Division, pubmed-meshheading:9927191-Clone Cells, pubmed-meshheading:9927191-Dexamethasone, pubmed-meshheading:9927191-Fusion Proteins, bcr-abl, pubmed-meshheading:9927191-Growth Inhibitors, pubmed-meshheading:9927191-Interleukin-6, pubmed-meshheading:9927191-Leukemia, Myelogenous, Chronic, BCR-ABL Positive, pubmed-meshheading:9927191-Leukemia Inhibitory Factor, pubmed-meshheading:9927191-Lymphokines, pubmed-meshheading:9927191-Macrophages, pubmed-meshheading:9927191-Mice, pubmed-meshheading:9927191-Phenotype, pubmed-meshheading:9927191-Proto-Oncogene Proteins c-myc, pubmed-meshheading:9927191-RNA, Messenger, pubmed-meshheading:9927191-Tumor Cells, Cultured
pubmed:year
1999
pubmed:articleTitle
Expression of BCR - ABL in M1 myeloid leukemia cells induces differentiation without arresting proliferation.
pubmed:affiliation
The Walter and Eliza Hall Institute of Medical Research and the Cooperative Research Centre for Cellular Growth Factors, Royal Melbourne Hospital, Victoria, Australia.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't