IGF-1R/epithelial-to-mesenchymal transition (EMT) crosstalk suppresses the erlotinib-sensitizing effect of EGFR exon 19 deletion mutations. - Wikidata - awgldk - TriplyDB

IGF-1R/epithelial-to-mesenchymal transition (EMT) crosstalk suppresses the erlotinib-sensitizing effect of EGFR exon 19 deletion mutations.

IGF-1R/epithelial-to-mesenchymal transition (EMT) crosstalk suppresses the erlotinib-sensitizing effect of EGFR exon 19 deletion mutations.

http://www.wikidata.org/entity/Q39101764

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Implications of Insulin-like Growth Factor 1 Receptor Activation in Lung Cancer The role of epithelial to mesenchymal transition in resistance to epidermal growth factor receptor tyrosine kinase inhibitors in non-small cell lung cancer Management of hyperglycemia from epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) targeting T790M-mediated resistance HRD1-Mediated IGF-1R Ubiquitination Contributes to Renal Protection of Resveratrol in db/db Mice.Molecular pathways and therapeutic targets in lung cancer Rationale for co-targeting IGF-1R and ALK in ALK fusion-positive lung cancer Crosstalk of Oncogenic Signaling Pathways during Epithelial-Mesenchymal Transition.Regulated genes in mesenchymal stem cells and gastric cancer Inactivation of GSK3β and activation of NF-κB pathway via Axl represents an important mediator of tumorigenesis in esophageal squamous cell carcinoma.Targeting insulin-like growth factor 1 receptor inhibits pancreatic cancer growth and metastasis.Linking tumor mutations to drug responses via a quantitative chemical-genetic interaction map.Insulin-like growth factor (IGF) signaling in tumorigenesis and the development of cancer drug resistance.Integrating Murine and Clinical Trials with Cabozantinib to Understand Roles of MET and VEGFR2 as Targets for Growth Inhibition of Prostate Cancer.Implication of epithelial-mesenchymal transition in IGF1R-induced resistance to EGFR-TKIs in advanced non-small cell lung cancer.Unique roles of Akt1 and Akt2 in IGF-IR mediated lung tumorigenesis.Silibinin suppresses EMT-driven erlotinib resistance by reversing the high miR-21/low miR-200c signature in vivo IGF-IR cooperates with ERα to inhibit breast cancer cell aggressiveness by regulating the expression and localisation of ECM molecules IGF-IR signaling in epithelial to mesenchymal transition and targeting IGF-IR therapy: overview and new insights Suppression of endogenous lipogenesis induces reversion of the malignant phenotype and normalized differentiation in breast cancer.PD 0332991, a selective cyclin D kinase 4/6 inhibitor, sensitizes lung cancer cells to treatment with epidermal growth factor receptor tyrosine kinase inhibitors.IGF1R depletion facilitates MET-amplification as mechanism of acquired resistance to erlotinib in HCC827 NSCLC cells.MET amplification and epithelial-to-mesenchymal transition exist as parallel resistance mechanisms in erlotinib-resistant, EGFR-mutated, NSCLC HCC827 cells Developmental pathways associated with cancer metastasis: Notch, Wnt, and Hedgehog.Inhibition of IGF1R signaling abrogates resistance to afatinib (BIBW2992) in EGFR T790M mutant lung cancer cells.Acquired Resistance to the Mutant-Selective EGFR Inhibitor AZD9291 Is Associated with Increased Dependence on RAS Signaling in Preclinical Models.The insulin-like growth factor 1 receptor causes acquired resistance to erlotinib in lung cancer cells with the wild-type epidermal growth factor receptor.Stem cell-like ALDH(bright) cellular states in EGFR-mutant non-small cell lung cancer: a novel mechanism of acquired resistance to erlotinib targetable with the natural polyphenol silibinin.Acquisition of EGFR TKI resistance and EMT phenotype is linked with activation of IGF1R/NF-κB pathway in EGFR-mutant NSCLC.Crosstalk between VEGFR and other receptor tyrosine kinases for TKI therapy of metastatic renal cell carcinoma.Mutations of EGFR or KRAS and expression of chemotherapy-related genes based on small biopsy samples in stage IIIB and IV inoperable non-small cell lung cancer.Molecular Signatures of the Insulin-like Growth Factor 1-mediated Epithelial-Mesenchymal Transition in Breast, Lung and Gastric Cancers

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IGF-1R/epithelial-to-mesenchymal transition (EMT) crosstalk suppresses the erlotinib-sensitizing effect of EGFR exon 19 deletion mutations.

http://www.wikidata.org/entity/Q39101764

description

2013 nî lūn-bûn

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2013年の論文

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2013年論文

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2013年論文

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2013年論文

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2013年論文

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2013年论文

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2013年论文

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2013年论文

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name

IGF-1R/epithelial-to-mesenchym ...... FR exon 19 deletion mutations.

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IGF-1R/epithelial-to-mesenchymal transition

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type

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IGF-1R/epithelial-to-mesenchym ...... FR exon 19 deletion mutations.

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IGF-1R/epithelial-to-mesenchymal transition

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prefLabel

IGF-1R/epithelial-to-mesenchym ...... FR exon 19 deletion mutations.

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IGF-1R/epithelial-to-mesenchymal transition

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Scientific Reports

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IGF-1R/epithelial-to-mesenchym ...... FR exon 19 deletion mutations.

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Alejandro Vazquez-Martin

http://www.w3.org/2001/XMLSchema#string

Bruna Corominas-Faja

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Cristina Oliveras-Ferraros

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Joana Visa

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Rosa Bonavia

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Sílvia Cufí

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Violeta Zenobia Torres-Garcia

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P2860

Aberrant expression of the transcription factors snail and slug alters the response to genotoxic stress

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

MET amplification occurs with or without T790M mutations in EGFR mutant lung tumors with acquired resistance to gefitinib or erlotinib

Acquired resistance of lung adenocarcinomas to gefitinib or erlotinib is associated with a second mutation in the EGFR kinase domain

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

EGFR mutation and resistance of non-small-cell lung cancer to gefitinib.

Exon 19 deletion mutations of epidermal growth factor receptor are associated with prolonged survival in non-small cell lung cancer patients treated with gefitinib or erlotinib.

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

Genotypic and histological evolution of lung cancers acquiring resistance to EGFR inhibitors

Activating mutations in the epidermal growth factor receptor underlying responsiveness of non-small-cell lung cancer to gefitinib

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10.1038/SREP02560

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3

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Enrique Barrajón-Catalán

Elisabet Cuyàs

Joaquim Bosch-Barrera

Javier A Menendez

Begoña Martin-Castillo

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2013-01-01T00:00:00Z

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256331637

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23994953

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