Linked Life Data

17329971

Source:http://linkedlifedata.com/resource/pubmed/id/17329971

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2007-3-12
pubmed:abstractText
Complex pathways exist in mammalian cells to regulate the expression and activity of oncogenes and tumor suppressor genes. Defining these regulatory pathways is an important step towards being able to interfere with tumorigenesis. Here we discuss our recent study indicating that activation of the phosphoinositide 3-kinase (PI3K) signaling pathway through inactivating mutations in PTEN or activating mutations in PIK3CA causes functional activation of p53 signaling in human cells.(1)ur data suggest that activation of p53 is a fail-safe mechanism triggered by loss of PTEN or oncogenic activation of PI3K, and furthermore, that these events provide selective pressure to mutate p53.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
1551-4005
pubmed:author
pubmed:issnType
Electronic
pubmed:day
15
pubmed:volume
6
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
394-6
pubmed:dateRevised
2011-9-22
pubmed:meshHeading
pubmed:year
2007
pubmed:articleTitle
Activated PI3K signaling as an endogenous inducer of p53 in human cancer.
pubmed:affiliation
Department of Oncology, Lombardi Comprehensive Cancer Center, Georgetown University School of Medicine, Washington, DC, USA.
pubmed:publicationType
Journal Article