Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2003-6-12
pubmed:abstractText
The p210 bcr-abl fusion protein has a key role in the pathogenesis of chronic myeloid leukemia (CML). However, its influence on disease progression to blast crisis is marginal and mostly due to its effect of impairing the genomic stability of clonal myeloid progenitors through pathways still largely unknown.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
1592-8721
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
88
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
622-30
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:12801837-Aneuploidy, pubmed-meshheading:12801837-Animals, pubmed-meshheading:12801837-CDC2 Protein Kinase, pubmed-meshheading:12801837-Cell Cycle, pubmed-meshheading:12801837-Clone Cells, pubmed-meshheading:12801837-Cyclin B, pubmed-meshheading:12801837-Fusion Proteins, bcr-abl, pubmed-meshheading:12801837-Gene Expression, pubmed-meshheading:12801837-Genome, pubmed-meshheading:12801837-Kinetics, pubmed-meshheading:12801837-Leukemia, Myelogenous, Chronic, BCR-ABL Positive, pubmed-meshheading:12801837-Mice, pubmed-meshheading:12801837-Myeloid Progenitor Cells, pubmed-meshheading:12801837-Oncogene Proteins, Viral, pubmed-meshheading:12801837-Ploidies, pubmed-meshheading:12801837-Polyploidy, pubmed-meshheading:12801837-Protein-Tyrosine Kinases, pubmed-meshheading:12801837-Repressor Proteins, pubmed-meshheading:12801837-Tumor Suppressor Protein p53
pubmed:year
2003
pubmed:articleTitle
p53 loss of function enhances genomic instability and accelerates clonal evolution of murine myeloid progenitors expressing the p(210)BCR-ABL tyrosine kinase.
pubmed:affiliation
Istituto di Ematologia e Oncologia Medica "Lorenzo e Ariosto Seràgnoli", University of Bologna Medical School, Bologna, Italy.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't