Source:http://linkedlifedata.com/resource/pubmed/id/17043013
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
11
|
| pubmed:dateCreated |
2006-11-3
|
| pubmed:abstractText |
Significant progress has been made in identifying genetic lesions that are causally implicated in the pathogenesis of acute myeloid leukemia (AML). These insights improve our understanding of the genetic basis of the disease, a prerequisite for the development of novel therapeutic approaches.
|
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:month |
Nov
|
| pubmed:issn |
1592-8721
|
| pubmed:author | |
| pubmed:issnType |
Electronic
|
| pubmed:volume |
91
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
1569-70
|
| pubmed:dateRevised |
2009-11-19
|
| pubmed:meshHeading | |
| pubmed:year |
2006
|
| pubmed:articleTitle |
JAK2V617F mutations as cooperative genetic lesions in t(8;21)-positive acute myeloid leukemia.
|
| pubmed:publicationType |
Letter,
Research Support, Non-U.S. Gov't
|