Knockin of mutant PIK3CA activates multiple oncogenic pathways
about
Phosphoinositides: tiny lipids with giant impact on cell regulationThe role of phosphoinositide-regulated actin reorganization in chemotaxis and cell migrationPIK3CA and AKT1 mutations have distinct effects on sensitivity to targeted pathway inhibitors in an isogenic luminal breast cancer model system.Active PI3K pathway causes an invasive phenotype which can be reversed or promoted by blocking the pathway at divergent nodesDifferential enhancement of breast cancer cell motility and metastasis by helical and kinase domain mutations of class IA phosphoinositide 3-kinase.Mutation site and context dependent effects of ESR1 mutation in genome-edited breast cancer cell models.The PI3K-Akt-mTOR pathway in initiation and progression of thyroid tumors.Caffeic acid derivatives inhibit the growth of colon cancer: involvement of the PI3-K/Akt and AMPK signaling pathwaysEngineering ePTEN, an enhanced PTEN with increased tumor suppressor activities.The phosphoinositide-3-kinase-Akt-mTOR pathway as a therapeutic target in breast cancerPIK3CA and KRAS mutations predict for response to everolimus therapy: now that's RAD001Akt and ERK control the proliferative response of mammary epithelial cells to the growth factors IGF-1 and EGF through the cell cycle inhibitor p57Kip2.Activation of diverse signalling pathways by oncogenic PIK3CA mutations.Multiple metabolic alterations exist in mutant PI3K cancers, but only glucose is essential as a nutrient sourceSimple monitoring of gene targeting efficiency in human somatic cell lines using the PIGA gene.Knock in of the AKT1 E17K mutation in human breast epithelial cells does not recapitulate oncogenic PIK3CA mutations.PIK3CA mutations and EGFR overexpression predict for lithium sensitivity in human breast epithelial cells.MACROD2 overexpression mediates estrogen independent growth and tamoxifen resistance in breast cancers.AKT-independent signaling downstream of oncogenic PIK3CA mutations in human cancerThe butterfly effect in cancer: a single base mutation can remodel the cell.A phosphoproteomic screen demonstrates differential dependence on HER3 for MAP kinase pathway activation by distinct PIK3CA mutations.Deletion of p53 in human mammary epithelial cells causes chromosomal instability and altered therapeutic responseThe mammalian target of rapamycin regulates cholesterol biosynthetic gene expression and exhibits a rapamycin-resistant transcriptional profile.A comparative analysis of constitutive promoters located in adeno-associated viral vectors.The phosphoinositide 3-kinase regulatory subunit p85alpha can exert tumor suppressor properties through negative regulation of growth factor signaling.Phosphatidylinositol 3-kinase pathway activation in breast cancer brain metastases.Phosphorylations of Serines 21/9 in Glycogen Synthase Kinase 3α/β Are Not Required for Cell Lineage Commitment or WNT Signaling in the Normal Mouse IntestineNDRG1 links p53 with proliferation-mediated centrosome homeostasis and genome stability.PIK3CA dependence and sensitivity to therapeutic targeting in urothelial carcinoma.Activating PIK3CA Mutations Induce an Epidermal Growth Factor Receptor (EGFR)/Extracellular Signal-regulated Kinase (ERK) Paracrine Signaling Axis in Basal-like Breast Cancer.Activating Mutations in PIK3CA Lead to Widespread Modulation of the Tyrosine Phosphoproteome.Quantification of PtdInsP3 molecular species in cells and tissues by mass spectrometry.Overexpression of lipid metabolism genes and PBX1 in the contralateral breasts of women with estrogen receptor-negative breast cancer.HER2 missense mutations have distinct effects on oncogenic signaling and migration.Alterations of EGFR, p53 and PTEN that mimic changes found in basal-like breast cancer promote transformation of human mammary epithelial cells.Mutations in PIK3CA sensitize breast cancer cells to physiologic levels of aspirinRecurrent AKT mutations in human cancers: functional consequences and effects on drug sensitivityLoss of PTEN induces microtentacles through PI3K-independent activation of cofilinKi-67 is required for maintenance of cancer stem cells but not cell proliferation.Single copies of mutant KRAS and mutant PIK3CA cooperate in immortalized human epithelial cells to induce tumor formation.
P2860
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P2860
Knockin of mutant PIK3CA activates multiple oncogenic pathways
description
2009 nî lūn-bûn
@nan
2009 թուականի Փետրուարին հրատարակուած գիտական յօդուած
@hyw
2009 թվականի փետրվարին հրատարակված գիտական հոդված
@hy
2009年の論文
@ja
2009年論文
@yue
2009年論文
@zh-hant
2009年論文
@zh-hk
2009年論文
@zh-mo
2009年論文
@zh-tw
2009年论文
@wuu
name
Knockin of mutant PIK3CA activates multiple oncogenic pathways
@ast
Knockin of mutant PIK3CA activates multiple oncogenic pathways
@en
Knockin of mutant PIK3CA activates multiple oncogenic pathways
@nl
type
label
Knockin of mutant PIK3CA activates multiple oncogenic pathways
@ast
Knockin of mutant PIK3CA activates multiple oncogenic pathways
@en
Knockin of mutant PIK3CA activates multiple oncogenic pathways
@nl
prefLabel
Knockin of mutant PIK3CA activates multiple oncogenic pathways
@ast
Knockin of mutant PIK3CA activates multiple oncogenic pathways
@en
Knockin of mutant PIK3CA activates multiple oncogenic pathways
@nl
P2093
P2860
P3181
P356
P1476
Knockin of mutant PIK3CA activates multiple oncogenic pathways
@en
P2093
Abde M Abukhdeir
Akina Tamaki
Bedri Karakas
Ben Ho Park
D Marc Rosen
David Cosgrove
Grace Wang
Hiroyuki Konishi
John P Gustin
Joseph P Garay
P2860
P304
P3181
P356
10.1073/PNAS.0813351106
P407
P50
P577
2009-02-24T00:00:00Z