Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
7
pubmed:dateCreated
1998-10-19
pubmed:abstractText
The interaction between p145(c-KIT) and p210(bcr-abl) in transduced cell lines, and the selective outgrowth of normal progenitors during long-term culture of chronic myeloid leukemia (CML) cells on stroma deficient in stem-cell factor (SCF) suggests that the response of CML cells to SCF may be abnormal. We examined the proliferative effect of SCF(100 ng/mL), provided as the sole stimulus, on individual CD34(+) cells from five normal donors and five chronic-phase CML patients. Forty-eight percent of isolated single CML CD34(+) cells proliferated after 6 days of culture to a mean of 18 cells, whereas only 8% of normal CD34(+) cells proliferated (mean number of cells generated was 4). SCF, as a single agent, supported the survival and expansion of colony-forming unit-granulocyte-macrophage (CFU-GM) from CML CD34(+)CD38(+) cells and the more primitive CML CD34(+)CD38(-) cells. These CFU-GM colonies were all bcr-abl positive, showing the specificity of SCF stimulation for the leukemic cell population. Coculture of CML and normal CD34(+) cells showed exclusive growth of Ph+ cells, suggesting that growth in SCF alone is not dependent on secretion of cytokines by CML cells. SCF augmentation of beta1-integrin-mediated adhesion of CML CD34(+) cells to fibronectin was not increased when compared with the effect on normal CD34(+) cells, suggesting that the proliferative and adhesive responses resulting from SCF stimulation are uncoupled. The increased proliferation may contribute to the accumulation of leukemic progenitors, which is a feature of CML.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0006-4971
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
92
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2461-70
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:9746786-Adult, pubmed-meshheading:9746786-Antigens, CD34, pubmed-meshheading:9746786-Bone Marrow, pubmed-meshheading:9746786-Cell Adhesion, pubmed-meshheading:9746786-Cell Division, pubmed-meshheading:9746786-Culture Media, Serum-Free, pubmed-meshheading:9746786-Female, pubmed-meshheading:9746786-Fibronectins, pubmed-meshheading:9746786-Fusion Proteins, bcr-abl, pubmed-meshheading:9746786-Hematopoietic Cell Growth Factors, pubmed-meshheading:9746786-Hematopoietic Stem Cells, pubmed-meshheading:9746786-Humans, pubmed-meshheading:9746786-Leukemia, Myelogenous, Chronic, BCR-ABL Positive, pubmed-meshheading:9746786-Male, pubmed-meshheading:9746786-Neoplasm Proteins, pubmed-meshheading:9746786-Neoplastic Stem Cells, pubmed-meshheading:9746786-Philadelphia Chromosome, pubmed-meshheading:9746786-Proto-Oncogene Proteins c-kit, pubmed-meshheading:9746786-Stem Cell Factor, pubmed-meshheading:9746786-Tumor Cells, Cultured, pubmed-meshheading:9746786-Tumor Stem Cell Assay
pubmed:year
1998
pubmed:articleTitle
Stem cell factor as a single agent induces selective proliferation of the Philadelphia chromosome positive fraction of chronic myeloid leukemia CD34(+) cells.
pubmed:affiliation
Leukemia Research Laboratory, Division of Haematology, Hanson Centre for Cancer Research, IMVS, Adelaide, SA, Australia. sarah.moore@invs.sa.gov.au
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't