Linked Life Data

10779439

Source:http://linkedlifedata.com/resource/pubmed/id/10779439

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
2000-5-23
pubmed:abstractText
The reciprocal translocation between chromosomes 9 and 22 that fuses coding sequences of the Bcr and Abl genes is responsible for a remarkably diverse group of hematologic malignancies. A newly described 230-kd form of Bcr-Abl has been associated with an indolent myeloproliferative syndrome referred to as chronic neutrophilic leukemia. We have cloned the corresponding gene and examined the biologic and biochemical properties of p230 Bcr-Abl after retroviral-mediated gene transfer into hematopoietic cell lines and primary bone marrow cells. p230 Bcr-Abl-expressing 32D myeloid cells were fully growth factor-independent and activated similar signal transduction pathways as the well-characterized p210 and p185 forms of Bcr-Abl. In contrast, primary mouse bone marrow cells expressing p230 required exogenous hematopoietic growth factors for optimal growth, whereas p185- and p210-expressing cells were independent of growth factors. The 3 Bcr-Abl proteins exerted different effects on differentiation of bone marrow cells. p185 induced outgrowth of lymphoid precursors capable of tumor formation in immunodeficient mice. In contrast, p210- and p230-expressing bone marrow cells caused limited outgrowth of lymphoid precursors that failed to form tumors in immunodeficient mice. Removal of cytokines and autologous stroma from Bcr-Abl-expressing bone marrow cultures produced the expansion of distinct lineages by the various Bcr-Abl proteins. p185 drove expansion of cytokine-independent lymphoid progenitors, while p210 and p230 generated cytokine-independent monocyte/myeloid cells. These findings suggest that the different Bcr-Abl fusion proteins drive the expansion of different hematopoietic populations, which may explain the association of the various Bcr-Abl oncoproteins with different spectra of human leukemias. (Blood. 2000;95:2913-2921)
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0006-4971
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
95
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2913-21
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:10779439-Animals, pubmed-meshheading:10779439-Antigens, Differentiation, pubmed-meshheading:10779439-Bone Marrow Cells, pubmed-meshheading:10779439-Cell Cycle, pubmed-meshheading:10779439-Cell Line, pubmed-meshheading:10779439-Cells, Cultured, pubmed-meshheading:10779439-Cloning, Molecular, pubmed-meshheading:10779439-Fusion Proteins, bcr-abl, pubmed-meshheading:10779439-Genes, abl, pubmed-meshheading:10779439-Green Fluorescent Proteins, pubmed-meshheading:10779439-Hematopoietic Stem Cells, pubmed-meshheading:10779439-Humans, pubmed-meshheading:10779439-Luminescent Proteins, pubmed-meshheading:10779439-Mice, pubmed-meshheading:10779439-Oncogenes, pubmed-meshheading:10779439-Protein-Tyrosine Kinases, pubmed-meshheading:10779439-Recombinant Fusion Proteins, pubmed-meshheading:10779439-Transfection, pubmed-meshheading:10779439-Tumor Cells, Cultured
pubmed:year
2000
pubmed:articleTitle
Analysis of the biologic properties of p230 Bcr-Abl reveals unique and overlapping properties with the oncogenic p185 and p210 Bcr-Abl tyrosine kinases.
pubmed:affiliation
Department of Pharmacology and Cancer Biology and the Divisions of Hematology and Oncology, Duke University Medical Center, Durham, NC 27710, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S., Research Support, Non-U.S. Gov't