ErbB-3 mediates phosphoinositide 3-kinase activity in gefitinib-sensitive non-small cell lung cancer cell lines. - Wikidata - awgldk - TriplyDB

ErbB-3 mediates phosphoinositide 3-kinase activity in gefitinib-sensitive non-small cell lung cancer cell lines.

ErbB-3 mediates phosphoinositide 3-kinase activity in gefitinib-sensitive non-small cell lung cancer cell lines.

http://www.wikidata.org/entity/Q33928631

about

Lyn, a Src family kinase, regulates activation of epidermal growth factor receptors in lung adenocarcinoma cells Transforming growth factor beta engages TACE and ErbB3 to activate phosphatidylinositol-3 kinase/Akt in ErbB2-overexpressing breast cancer and desensitizes cells to trastuzumab Perturbation of the mutated EGFR interactome identifies vulnerabilities and resistance mechanisms Activation of ERBB2 signaling causes resistance to the EGFR-directed therapeutic antibody cetuximab Intratumoral epiregulin is a marker of advanced disease in non-small cell lung cancer patients and confers invasive properties on EGFR-mutant cells MET amplification occurs with or without T790M mutations in EGFR mutant lung tumors with acquired resistance to gefitinib or erlotinib BIBW2992, an irreversible EGFR/HER2 inhibitor highly effective in preclinical lung cancer models Loss of Phosphatase and Tensin homologue deleted on chromosome 10 engages ErbB3 and insulin-like growth factor-I receptor signaling to promote antiestrogen resistance in breast cancer Met receptor acts uniquely for survival and morphogenesis of EGFR-dependent normal mammary epithelial and cancer cells Structures of Lung Cancer-Derived EGFR Mutants and Inhibitor Complexes: Mechanism of Activation and Insights into Differential Inhibitor Sensitivity An ATP-Competitive Inhibitor Modulates the Allosteric Function of the HER3 Pseudokinase Allelic dilution obscures detection of a biologically significant resistance mutation in EGFR-amplified lung cancer.Genotypic and histological evolution of lung cancers acquiring resistance to EGFR inhibitors Receptor tyrosine kinases exert dominant control over PI3K signaling in human KRAS mutant colorectal cancers.ROS1 rearrangements define a unique molecular class of lung cancers.Mechanisms of acquired crizotinib resistance in ALK-rearranged lung Cancers.Reactivation of ERK signaling causes resistance to EGFR kinase inhibitors.Primary concomitant EGFR T790M mutation predicted worse prognosis in non-small cell lung cancer patients Pharmacogenomics of EGFR-targeted therapies in non-small cell lung cancer: EGFR and beyond EGFR-TKI resistance in NSCLC patients: mechanisms and strategies HER2 oncogenic function escapes EGFR tyrosine kinase inhibitors via activation of alternative HER receptors in breast cancer cells High expression levels of total IGF-1R and sensitivity of NSCLC cells in vitro to an anti-IGF-1R antibody (R1507)A neutralizing RNA aptamer against EGFR causes selective apoptotic cell death PI3K pathway alterations in cancer: variations on a theme Targeting the phosphoinositide 3-kinase pathway in cancer Altered serine/threonine kinase activity in schizophrenia Aberrant trafficking of NSCLC-associated EGFR mutants through the endocytic recycling pathway promotes interaction with Src.Clinical benefit of readministration of gefitinib for initial gefitinib-responders with non-small cell lung cancer.Transcriptional profiling of non-small cell lung cancer cells with activating EGFR somatic mutations.High resolution melting analysis for rapid and sensitive EGFR and KRAS mutation detection in formalin fixed paraffin embedded biopsies.ERBB receptors: from oncogene discovery to basic science to mechanism-based cancer therapeutics.Discovery of AZD8931, an Equipotent, Reversible Inhibitor of Signaling by EGFR, HER2, and HER3 Receptors.Enhancement of gefitinib-induced growth inhibition by Marsdenia tenacissima extract in non-small cell lung cancer cells expressing wild or mutant EGFR.HER kinase axis receptor dimer partner switching occurs in response to EGFR tyrosine kinase inhibition despite failure to block cellular proliferation Amphiregulin promotes BAX inhibition and resistance to gefitinib in non-small-cell lung cancers.An ErbB3 antibody, MM-121, is active in cancers with ligand-dependent activation Combining phage and staphylococcal surface display for generation of ErbB3-specific Affibody molecules.Amplification of EGFR T790M causes resistance to an irreversible EGFR inhibitor Structural and mechanistic underpinnings of the differential drug sensitivity of EGFR mutations in non-small cell lung cancer.Mutational profiling reveals PIK3CA mutations in gallbladder carcinoma.

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P2860

ErbB-3 mediates phosphoinositide 3-kinase activity in gefitinib-sensitive non-small cell lung cancer cell lines.

http://www.wikidata.org/entity/Q33928631

description

2005 nî lūn-bûn

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2005 թուականի Փետրուարին հրատարակուած գիտական յօդուած

@hyw

2005 թվականի փետրվարին հրատարակված գիտական հոդված

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2005年の論文

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2005年論文

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2005年論文

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2005年論文

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2005年論文

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2005年論文

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2005年论文

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name

ErbB-3 mediates phosphoinositi ...... l cell lung cancer cell lines.

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ErbB-3 mediates phosphoinositi ...... l cell lung cancer cell lines.

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type

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ErbB-3 mediates phosphoinositi ...... l cell lung cancer cell lines.

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ErbB-3 mediates phosphoinositi ...... l cell lung cancer cell lines.

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ErbB-3 mediates phosphoinositi ...... l cell lung cancer cell lines.

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ErbB-3 mediates phosphoinositi ...... l cell lung cancer cell lines.

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Proceedings of the National Academy of Sciences of the United States of America

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ErbB-3 mediates phosphoinositi ...... l cell lung cancer cell lines.

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Bruce E Johnson

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Christina Fleet

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Jeffrey A Engelman

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Joseph Pearlberg

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Karen Cichowski

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Toru Mukohara

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P2860

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

Scansite 2.0: Proteome-wide prediction of cell signaling interactions using short sequence motifs

The ErbB2/ErbB3 heterodimer functions as an oncogenic unit: ErbB2 requires ErbB3 to drive breast tumor cell proliferation

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

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

Gefitinib-sensitizing EGFR mutations in lung cancer activate anti-apoptotic pathways

Acute mutation of retinoblastoma gene function is sufficient for cell cycle re-entry

The relationship between human epidermal growth-like factor receptor expression and cellular transformation in NIH3T3 cells

Oncogenes and signal transduction

Comparison of four chemotherapy regimens for advanced non-small-cell lung cancer

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102

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Lewis C. Cantley

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