Linked Life Data

19010541

Source:http://linkedlifedata.com/resource/pubmed/id/19010541

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2009-3-9
pubmed:abstractText
The biological hallmark of juvenile myelomonocytic leukemia (JMML) is selective GM-CSF hypersensitivity. We hypothesized that PTEN protein deficiency might lead to insufficient negative growth signals to counter the hyperactive Ras signaling and therefore aid in the acceleration of the malignant transformation of JMML. In screening 34 JMML patients we found: (1) decreased PTEN protein in 67% of patients; (2) significantly lower PTEN mRNA levels in patients compared to controls (p<0.01); (3) a hypermethylated PTEN promoter in 77% of patients; and (4) constitutive-hyperactive Akt and MAPK in 55% and 73% of patients, respectively. These findings suggest that PTEN deficiency is very common in JMML and is in part due to hypermethylation of the PTEN gene promoter.
pubmed:grant
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
1873-5835
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
33
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
671-7
pubmed:dateRevised
2011-9-22
pubmed:meshHeading
pubmed:year
2009
pubmed:articleTitle
PTEN deficiency is a common defect in juvenile myelomonocytic leukemia.
pubmed:affiliation
Winthrop P. Rockefeller Cancer Institute, University of Arkansas for Medical Sciences, 4301 West Markham Street, slot #623, Little Rock, AR 72205-7199, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural