Therapeutic destruction of insulin receptor substrates for cancer treatment. - Wikidata - wikimedia - TriplyDB

Therapeutic destruction of insulin receptor substrates for cancer treatment.

Therapeutic destruction of insulin receptor substrates for cancer treatment.

http://www.wikidata.org/entity/Q35343877

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Pathways and therapeutic targets in melanoma The struggle by Caenorhabditis elegans to maintain proteostasis during aging and disease The Novel Functions of High-Molecular-Mass Complexes Containing Insulin Receptor Substrates in Mediation and Modulation of Insulin-Like Activities: Emerging Concept of Diverse Functions by IRS-Associated Proteins CDK4 is an essential insulin effector in adipocytes Lack of association between insulin receptor substrate2 rs1805097 polymorphism and the risk of colorectal and breast cancer: a meta-analysis.IGF-I regulates redox status in breast cancer cells by activating the amino acid transport molecule xC-.IRS-2 rs1805097 polymorphism is associated with the decreased risk of colorectal cancer MiR-570 inhibits cell proliferation and glucose metabolism by targeting IRS1 and IRS2 in human chronic myelogenous leukemia.Role of insulin receptor substrates in the progression of hepatocellular carcinoma.PHIPing out: a genetic basis for tumor ulceration.Phosphoproteomic Analysis of Cell-Based Resistance to BRAF Inhibitor Therapy in Melanoma.Alcohol Consumption Modulates Host Defense in Rhesus Macaques by Altering Gene Expression in Circulating Leukocytes.Tissue and serum IGFBP7 protein as biomarker in high-grade soft tissue sarcoma Targeting colorectal cancer via its microenvironment by inhibiting IGF-1 receptor-insulin receptor substrate and STAT3 signaling.IRS2 silencing increases apoptosis and potentiates the effects of ruxolitinib in JAK2V617F-positive myeloproliferative neoplasms.CUDC-101, a Novel Inhibitor of Full-Length Androgen Receptor (flAR) and Androgen Receptor Variant 7 (AR-V7) Activity: Mechanism of Action and In Vivo Efficacy microRNA-7-5p inhibits melanoma cell proliferation and metastasis by suppressing RelA/NF-κB.Role of the polypeptide N-acetylgalactosaminyltransferase 3 in ovarian cancer progression: possible implications in abnormal mucin O-glycosylation.Worming our way to novel drug discovery with the Caenorhabditis elegans proteostasis network, stress response and insulin-signaling pathways.Minireview: Were the IGF Signaling Inhibitors All Bad?Suppression of B-Raf(V600E) cancers by MAPK hyper-activation PTEN regulates IGF-1R-mediated therapy resistance in melanoma.A novel inhibitor of the insulin/IGF signaling pathway protects from age-onset, neurodegeneration-linked proteotoxicity.Mixed Mesonephric Adenocarcinoma and High-grade Neuroendocrine Carcinoma of the Uterine Cervix: Case Description of a Previously Unreported Entity With Insights Into Its Molecular Pathogenesis.Preclinical Effectiveness of Selective Inhibitor of IRS-1/2 NT157 in Osteosarcoma Cell Lines.Bis-anthracycline WP760 abrogates melanoma cell growth by transcription inhibition, p53 activation and IGF1R downregulation.Trial Watch: Peptide vaccines in cancer therapy.Single nucleotide polymorphisms in the IGF-IRS pathway are associated with outcome in mCRC patients enrolled in the FIRE-3 trial.LPIN1 promotes epithelial cell transformation and mammary tumourigenesis via enhancing insulin receptor substrate 1 stability.Revisiting the IGF-1R as a breast cancer target.Targeting melanoma with NT157 by blocking Stat3 and IGF1R signaling.An exon variant in insulin receptor gene is associated with susceptibility to colorectal cancer in women.Postprandial increase in serum CA125 as a surrogate biomarker for early diagnosis of ovarian cancer.miR-130a and miR-145 reprogram Gr-1+CD11b+ myeloid cells and inhibit tumor metastasis through improved host immunity.New susceptibility loci for cutaneous melanoma risk and progression revealed using a porcine model.Association of IRS2 overexpression with disease progression in intrahepatic cholangiocarcinoma

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Therapeutic destruction of insulin receptor substrates for cancer treatment.

http://www.wikidata.org/entity/Q35343877

description

2013 nî lūn-bûn

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2013 թուականի Մայիսին հրատարակուած գիտական յօդուած

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2013 թվականի մայիսին հրատարակված գիտական հոդված

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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年論文

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2013年论文

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name

Therapeutic destruction of insulin receptor substrates for cancer treatment.

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Therapeutic destruction of insulin receptor substrates for cancer treatment.

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Therapeutic destruction of insulin receptor substrates for cancer treatment.

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Therapeutic destruction of insulin receptor substrates for cancer treatment.

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Therapeutic destruction of insulin receptor substrates for cancer treatment.

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Therapeutic destruction of insulin receptor substrates for cancer treatment.

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0008-5472.CAN-12-3385

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Cancer Research

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Therapeutic destruction of insulin receptor substrates for cancer treatment.

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Alexander Levitzki

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Alexei Shir

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Efrat Flashner-Abramson

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Hadas Reuveni

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Kirill Makedonski

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Lilach Steiner

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Menashe Bar-Eli

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Renduo Song

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P2860

Non-SH2 domains within insulin receptor substrate-1 and SHC mediate their phosphotyrosine-dependent interaction with the NPEY motif of the insulin-like growth factor I receptor

Clinical efficacy of a RAF inhibitor needs broad target blockade in BRAF-mutant melanoma

PLX4032, a selective BRAF(V600E) kinase inhibitor, activates the ERK pathway and enhances cell migration and proliferation of BRAF melanoma cells

Silencing cAMP-response element-binding protein (CREB) identifies CYR61 as a tumor suppressor gene in melanoma

Mammary tumorigenesis and metastasis caused by overexpression of insulin receptor substrate 1 (IRS-1) or IRS-2

Inhibition of Mutated, Activated BRAF in Metastatic Melanoma

Expression of the type 1 insulin-like growth factor receptor is up-regulated in primary prostate cancer and commonly persists in metastatic disease

Raf kinases in cancer-roles and therapeutic opportunities

Insulin-like growth factor-I receptor signalling and acquired resistance to gefitinib (ZD1839; Iressa) in human breast and prostate cancer cells

Acquired resistance to BRAF inhibitors mediated by a RAF kinase switch in melanoma can be overcome by cotargeting MEK and IGF-1R/PI3K

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4383-4394

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scholarly article

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10.1158/0008-5472.CAN-12-3385

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14

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73

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Meenhard Herlyn

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2013-05-07T00:00:00Z

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23651636

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