Linked Life Data

17658267

Source:http://linkedlifedata.com/resource/pubmed/id/17658267

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2007-8-6
pubmed:abstractText
Acute myeloid leukemia (AML) is a quickly progressing, heterogeneous clonal disorder of hematopoietic progenitor cells. Significant progress in understanding the pathogenesis of AML has been achieved in the past few years. Two major types of genetic events are thought to give rise to leukemic transformation: alterations in the activity of transcription factors controlling hematopoietic differentiation and activation of components of receptor tyrosine kinase (RTK) signaling pathways. This has led to the development of promising new therapeutic strategies for the disease. In this article, we will discuss recent developments in the field of molecularly targeted therapies for AML, which involve RTKs such as FMS-like tyrosine kinase 3 (Flt3), c-Kit and signal transduction via the phosphoinositide 3-kinase (PI3K) and mitogen-activated protein kinase (MAPK) pathways. Initial results imply that targeting RTKs is a very promising approach for AML and that other receptors, such as the insulin-like growth factor receptor (IGF-IR), could also represent new targets in the future.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
1040-8428
pubmed:author
pubmed:issnType
Print
pubmed:volume
63
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
215-30
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:year
2007
pubmed:articleTitle
Targeting receptor tyrosine kinase signaling in acute myeloid leukemia.
pubmed:affiliation
Division of Clinical Chemistry and Biochemistry, University Children's Hospital Zurich, Steinwiesstrasse 75, CH-8032 Zurich, Switzerland.
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't