Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
2006-5-15
pubmed:abstractText
The potential oncogenicity of PI 3-kinases is revealed by two principal mechanisms: mutations causing gain of function and overexpression of wild-type proteins. Cancer-specific mutations in PIK3CA, the gene coding for the catalytic subunit p110alpha of PI 3-kinase, are oncogenic in the animal. These mutations are therefore significant determinants of the oncogenic cellular phenotype in human tumors and are appropriate and promising targets for small molecule inhibitors. Overexpression of wild-type p110beta, gamma and delta induces oncogenic transformation in cell culture. Although these non-alpha isoforms of PI 3-kinase have not been found mutated in human cancer, deregulated expression could contribute to cellular oncogenic properties and deserves increased attention.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
1551-4005
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
5
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
946-9
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed:year
2006
pubmed:articleTitle
PI 3-kinases: hidden potentials revealed.
pubmed:affiliation
Department of Molecular and Experimental Medicine, The Scripps Research Institute, La Jolla, California 92037, USA. pkvogt@scripps.edu
pubmed:publicationType
Journal Article, Research Support, N.I.H., Extramural