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dc.contributor.authorMorrow, Christopher J
dc.contributor.authorGray, Alexander
dc.contributor.authorDive, Caroline
dc.date.accessioned2009-07-24T15:17:37Z
dc.date.available2009-07-24T15:17:37Z
dc.date.issued2005-09-26
dc.identifier.citationComparison of phosphatidylinositol-3-kinase signalling within a panel of human colorectal cancer cell lines with mutant or wild-type PIK3CA. 2005, 579 (23):5123-8 FEBS Lett.en
dc.identifier.issn0014-5793
dc.identifier.pmid16150444
dc.identifier.doi10.1016/j.febslet.2005.07.096
dc.identifier.urihttp://hdl.handle.net/10541/75653
dc.description.abstractRecent studies have identified conserved missense mutations in PIK3CA, the gene encoding the catalytic phosphatidylinositol-3-kinase subunit p110alpha, in a variety of human cancers. Further investigation demonstrated that PIK3CA mutations lead to increased basal phosphatidylinositol-3-kinase activity, promoting cell growth and invasion [Samuels, Y., Diaz, L.A., Jr., Schmidt-Kittler, O., Cummins, J.M., Delong, L., Cheong, I., Rago, C., Huso, D.L., Lengauer, C., Kinzler, K.W., Vogelstein, B. and Velculescu, V.E. (2005) Mutant PIK3CA promotes cell growth and invasion of human cancer cells. Cancer Cell 7, 561-573]. A panel of commonly used colorectal cancer cell lines was screened for these PIK3CA mutations. Constitutive and IGF-1-stimulated phosphatidylinositol-3-kinase activity, signal response and duration were assessed. In the assays used no differences distinguished cells carrying PIK3CA mutations indicating that these mutations did not significantly alter growth factor stimulated or steady state phosphatidylinositol-3-kinase activity in normal cell culture conditions.
dc.language.isoenen
dc.subjectCell Line Tumouren
dc.subjectTumour Markersen
dc.subjectColorectal Canceren
dc.subject.mesh1-Phosphatidylinositol 3-Kinase
dc.subject.meshCell Line, Tumor
dc.subject.meshColorectal Neoplasms
dc.subject.meshDNA Mutational Analysis
dc.subject.meshHumans
dc.subject.meshInsulin-Like Growth Factor I
dc.subject.meshSignal Transduction
dc.subject.meshTumor Markers, Biological
dc.titleComparison of phosphatidylinositol-3-kinase signalling within a panel of human colorectal cancer cell lines with mutant or wild-type PIK3CA.en
dc.typeArticleen
dc.contributor.departmentCellular and Molecular Pharmacology Group, Paterson Institute for Cancer Research, Christie Hospital NHS Trust, Wilmslow Road, Withington, Manchester M20 4BX, United Kingdom.en
dc.identifier.journalFEBS Lettersen
html.description.abstractRecent studies have identified conserved missense mutations in PIK3CA, the gene encoding the catalytic phosphatidylinositol-3-kinase subunit p110alpha, in a variety of human cancers. Further investigation demonstrated that PIK3CA mutations lead to increased basal phosphatidylinositol-3-kinase activity, promoting cell growth and invasion [Samuels, Y., Diaz, L.A., Jr., Schmidt-Kittler, O., Cummins, J.M., Delong, L., Cheong, I., Rago, C., Huso, D.L., Lengauer, C., Kinzler, K.W., Vogelstein, B. and Velculescu, V.E. (2005) Mutant PIK3CA promotes cell growth and invasion of human cancer cells. Cancer Cell 7, 561-573]. A panel of commonly used colorectal cancer cell lines was screened for these PIK3CA mutations. Constitutive and IGF-1-stimulated phosphatidylinositol-3-kinase activity, signal response and duration were assessed. In the assays used no differences distinguished cells carrying PIK3CA mutations indicating that these mutations did not significantly alter growth factor stimulated or steady state phosphatidylinositol-3-kinase activity in normal cell culture conditions.


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