Replacement of normal with mutant alleles in the genome of normal human cells unveils mutation-specific drug responses
about
Deregulation of the PI3K and KRAS signaling pathways in human cancer cells determines their response to everolimusEmergence of KRAS mutations and acquired resistance to anti-EGFR therapy in colorectal cancerIn vitro human cell line models to predict clinical response to anticancer drugsIn vitro and in vivo models for analysis of resistance to anticancer molecular therapiesPIK3CA and AKT1 mutations have distinct effects on sensitivity to targeted pathway inhibitors in an isogenic luminal breast cancer model system.CDK1 Is a Synthetic Lethal Target for KRAS Mutant Tumours.KRAS gene amplification in colorectal cancer and impact on response to EGFR-targeted therapyActivation of β-catenin by oncogenic PIK3CA and EGFR promotes resistance to glucose deprivation by inducing a strong antioxidant responseActive PI3K pathway causes an invasive phenotype which can be reversed or promoted by blocking the pathway at divergent nodesSystematic analysis of genotype-specific drug responses in cancer.CanProVar: a human cancer proteome variation database.PIK3CA and KRAS mutations predict for response to everolimus therapy: now that's RAD001Simple monitoring of gene targeting efficiency in human somatic cell lines using the PIGA gene.Cockayne syndrome group B protein regulates DNA double-strand break repair and checkpoint activation.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.Personalizing health care: feasibility and future implications.Multi-kilobase homozygous targeted gene replacement in human induced pluripotent stem cells.Targeting oncogenic serine/threonine-protein kinase BRAF in cancer cells inhibits angiogenesis and abrogates hypoxia.Absolute Quantification of Endogenous Ras Isoform AbundanceHER2 missense mutations have distinct effects on oncogenic signaling and migration.The role of EGFR monoclonal antibodies (MoABs) cetuximab/panitumab, and BRAF inhibitors in BRAF mutated colorectal cancer.Alterations of EGFR, p53 and PTEN that mimic changes found in basal-like breast cancer promote transformation of human mammary epithelial cells.Signaling via class IA Phosphoinositide 3-kinases (PI3K) in human, breast-derived cell linesComputational drugs repositioning identifies inhibitors of oncogenic PI3K/AKT/P70S6K-dependent pathways among FDA-approved compounds.Oncogene-Selective Sensitivity to Synchronous Cell Death following Modulation of the Amino Acid Nutrient Cystine.The Consequences of Chromosome Segregation Errors in Mitosis and Meiosis.Challenges and opportunities for cell line secretomes in cancer proteomics.The development of high-content screening (HCS) technology and its importance to drug discovery.Improved methods of AAV-mediated gene targeting for human cell lines using ribosome-skipping 2A peptide.KRAS exon 2 mutations influence activity of regorafenib in an SW48-based disease model of colorectal cancer.Targeted knock-in of the polymorphism rs61764370 does not affect KRAS expression but reduces let-7 levels.Through a glass darkly: economics and personalised medicine.A requirement for wild-type Ras isoforms in mutant KRas-driven signalling and transformation.KRAS allel-specific activity of sunitinib in an isogenic disease model of colorectal cancer.Modeling tumor progression by the sequential introduction of genetic alterations into the genome of human normal cells.Identification of mutant K-Ras-dependent phenotypes using a panel of isogenic cell lines.MM-151 overcomes acquired resistance to cetuximab and panitumumab in colorectal cancers harboring EGFR extracellular domain mutations.Multi-marker analysis of circulating cell-free DNA toward personalized medicine for colorectal cancerOncogenic KRAS sensitizes premalignant, but not malignant cells, to Noxa-dependent apoptosis through the activation of the MEK/ERK pathway.
P2860
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P2860
Replacement of normal with mutant alleles in the genome of normal human cells unveils mutation-specific drug responses
description
2008 nî lūn-bûn
@nan
2008 թուականի Դեկտեմբերին հրատարակուած գիտական յօդուած
@hyw
2008 թվականի դեկտեմբերին հրատարակված գիտական հոդված
@hy
2008年の論文
@ja
2008年学术文章
@wuu
2008年学术文章
@zh-cn
2008年学术文章
@zh-hans
2008年学术文章
@zh-my
2008年学术文章
@zh-sg
2008年學術文章
@yue
name
Replacement of normal with mut ...... tation-specific drug responses
@ast
Replacement of normal with mut ...... tation-specific drug responses
@en
Replacement of normal with mut ...... tation-specific drug responses
@nl
type
label
Replacement of normal with mut ...... tation-specific drug responses
@ast
Replacement of normal with mut ...... tation-specific drug responses
@en
Replacement of normal with mut ...... tation-specific drug responses
@nl
prefLabel
Replacement of normal with mut ...... tation-specific drug responses
@ast
Replacement of normal with mut ...... tation-specific drug responses
@en
Replacement of normal with mut ...... tation-specific drug responses
@nl
P2093
P2860
P50
P356
P1476
Replacement of normal with mut ...... tation-specific drug responses
@en
P2093
Carlotta Cancelliere
Davide Zecchin
Giulia Maria Stella
Margherita Gallicchio
Massimo Geuna
Simona Emilia Flonta
Simona Lamba
P2860
P304
P356
10.1073/PNAS.0808757105
P407
P50
P577
2008-12-30T00:00:00Z