Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
2004-3-23
pubmed:abstractText
Since its introduction less than 3 years ago, imatinib mesylate (STI571) has altered the entire approach to the therapy of patients with chronic myeloid leukemia (CML). In addition to its impact on clinical practice, imatinib has also increased the focus of basic and translational CML research on enhancing the cellular effects of imatinib and preventing and overcoming resistance to the drug. Here, I summarize some recent advances in our understanding of the regulatory and signaling mechanisms of Bcr-Abl, with an emphasis on therapeutic implications.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0145-2126
pubmed:author
pubmed:issnType
Print
pubmed:volume
28 Suppl 1
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
S21-8
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
2004
pubmed:articleTitle
Mechanisms of transformation by the BCR-ABL oncogene: new perspectives in the post-imatinib era.
pubmed:affiliation
Molecular Oncology Research Institute, Tufts-New England Medical Center, 750 Washington Street, Boston, MA 02111, USA. rvanetten@tufts-nemc.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Review