Receptor tyrosine kinases exert dominant control over PI3K signaling in human KRAS mutant colorectal cancers. - Wikidata - wikimedia - TriplyDB

Receptor tyrosine kinases exert dominant control over PI3K signaling in human KRAS mutant colorectal cancers.

Receptor tyrosine kinases exert dominant control over PI3K signaling in human KRAS mutant colorectal cancers.

http://www.wikidata.org/entity/Q27851674

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Primary and acquired resistance to EGFR-targeted therapies in colorectal cancer: impact on future treatment strategies Landscape of Targeted Anti-Cancer Drug Synergies in Melanoma Identifies a Novel BRAF-VEGFR/PDGFR Combination Treatment CIViC database Metastasis-associated PRL-3 induces EGFR activation and addiction in cancer cells RAS Synthetic Lethal Screens Revisited: Still Seeking the Elusive Prize?Targeting Cdc42 with the small molecule drug AZA197 suppresses primary colon cancer growth and prolongs survival in a preclinical mouse xenograft model by downregulation of PAK1 activity Synergistic effects of combined Wnt/KRAS inhibition in colorectal cancer cells Synergistic effects of targeted PI3K signaling inhibition and chemotherapy in liposarcoma Harnessing Connectivity in a Large-Scale Small-Molecule Sensitivity Dataset.KRAS-dependent suppression of MYC enhances the sensitivity of cancer cells to cytotoxic agents.ERBB receptors: from oncogene discovery to basic science to mechanism-based cancer therapeutics.PI3K isoform dependence of PTEN-deficient tumors can be altered by the genetic context.ZEB1 sensitizes lung adenocarcinoma to metastasis suppression by PI3K antagonism.Activated cMET and IGF1R-driven PI3K signaling predicts poor survival in colorectal cancers independent of KRAS mutational status.Inhibition of fatty acid synthase induces pro-survival Akt and ERK signaling in K-Ras-driven cancer cells.Change or die: targeting adaptive signaling to kinase inhibition in cancer cells.Upregulation of IGF1R by mutant RAS in leukemia and potentiation of RAS signaling inhibitors by small-molecule inhibition of IGF1R Patient-derived models of acquired resistance can identify effective drug combinations for cancer.Not just gRASping at flaws: finding vulnerabilities to develop novel therapies for treating KRAS mutant cancers Concurrent Targeting of KRAS and AKT by MiR-4689 Is a Novel Treatment Against Mutant KRAS Colorectal Cancer.Drugging the undruggable RAS: Mission possible?Phosphoproteomic analysis of basal and therapy-induced adaptive signaling networks in BRAF and NRAS mutant melanoma.Trametinib with or without vemurafenib in BRAF mutated non-small cell lung cancer.Genetic events that limit the efficacy of MEK and RTK inhibitor therapies in a mouse model of KRAS-driven pancreatic cancer EGFR-mediated re-activation of MAPK signaling contributes to insensitivity of BRAF mutant colorectal cancers to RAF inhibition with vemurafenib The role of phosphoinositide 3-kinase signaling in intestinal inflammation Dual inactivation of Akt and ERK by TIC10 signals Foxo3a nuclear translocation, TRAIL gene induction, and potent antitumor effects.K-Ras mutation-mediated IGF-1-induced feedback ERK activation contributes to the rapalog resistance in pancreatic ductal adenocarcinomas.A central role for RAF→MEK→ERK signaling in the genesis of pancreatic ductal adenocarcinoma.PIK3CA mutation H1047R is associated with response to PI3K/AKT/mTOR signaling pathway inhibitors in early-phase clinical trials KRAS insertion mutations are oncogenic and exhibit distinct functional properties.Targeted therapies in colorectal cancer-an integrative view by PPPM Colorectal cancer carcinogenesis: a review of mechanisms Defective K-Ras oncoproteins overcome impaired effector activation to initiate leukemia in vivo Combined PI3K/mTOR and MEK inhibition provides broad antitumor activity in faithful murine cancer models Epithelial-to-Mesenchymal Transition Defines Feedback Activation of Receptor Tyrosine Kinase Signaling Induced by MEK Inhibition in KRAS-Mutant Lung Cancer.MicroRNA-543 suppresses colorectal cancer growth and metastasis by targeting KRAS, MTA1 and HMGA2.Enhanced anti-tumour activity of the combination of the novel MEK inhibitor WX-554 and the novel PI3K inhibitor WX-037.PI3K regulates MEK/ERK signaling in breast cancer via the Rac-GEF, P-Rex1.Bypass mechanisms of resistance to receptor tyrosine kinase inhibition in lung cancer.

P2860

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P2860

Receptor tyrosine kinases exert dominant control over PI3K signaling in human KRAS mutant colorectal cancers.

http://www.wikidata.org/entity/Q27851674

description

2011 nî lūn-bûn

@nan

2011 թուականի Նոյեմբերին հրատարակուած գիտական յօդուած

@hyw

2011 թվականի նոյեմբերին հրատարակված գիտական հոդված

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2011年の論文

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2011年論文

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2011年論文

@zh-hant

2011年論文

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2011年論文

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2011年論文

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2011年论文

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name

Receptor tyrosine kinases exer ...... RAS mutant colorectal cancers.

@ast

Receptor tyrosine kinases exer ...... RAS mutant colorectal cancers.

@en

Receptor tyrosine kinases exer ...... RAS mutant colorectal cancers.

@nl

type

label

Receptor tyrosine kinases exer ...... RAS mutant colorectal cancers.

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Receptor tyrosine kinases exer ...... RAS mutant colorectal cancers.

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Receptor tyrosine kinases exer ...... RAS mutant colorectal cancers.

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altLabel

Receptor tyrosine kinases exer ...... KRAS mutant colorectal cancers

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prefLabel

Receptor tyrosine kinases exer ...... RAS mutant colorectal cancers.

@ast

Receptor tyrosine kinases exer ...... RAS mutant colorectal cancers.

@en

Receptor tyrosine kinases exer ...... RAS mutant colorectal cancers.

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Journal of Clinical Investigation

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Receptor tyrosine kinases exer ...... RAS mutant colorectal cancers.

@en

P2093

Anurag Singh

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Cyril Benes

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David P Ryan

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Eugene Lifshits

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Hiromichi Ebi

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Jeffrey A Engelman

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Jeffrey Settleman

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Lewis C Cantley

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Ryan B Corcoran

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Youngchul Song

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P2860

KRAS mutations and primary resistance of lung adenocarcinomas to gefitinib or erlotinib

Binding of ras to phosphoinositide 3-kinase p110alpha is required for ras-driven tumorigenesis in mice

Normal and oncogenic p21ras proteins bind to the amino-terminal regulatory domain of c-Raf-1

EGF receptor gene mutations are common in lung cancers from "never smokers" and are associated with sensitivity of tumors to gefitinib and erlotinib

Integrative genomic and proteomic analyses identify targets for Lkb1-deficient metastatic lung tumors

Crystal structure and functional analysis of Ras binding to its effector phosphoinositide 3-kinase gamma

Use of chemotherapy plus a monoclonal antibody against HER2 for metastatic breast cancer that overexpresses HER2.

EGFR mutations in lung cancer: correlation with clinical response to gefitinib therapy.

KRAS mutation status is predictive of response to cetuximab therapy in colorectal cancer.

MET amplification leads to gefitinib resistance in lung cancer by activating ERBB3 signaling.

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4311-21

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scholarly article

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10.1172/JCI57909

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11

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121

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Jeffrey A Meyerhardt

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2011-11-01T00:00:00Z

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21985784

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3204842

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