MEK-ERK signaling dictates DNA-repair gene MGMT expression and temozolomide resistance of stem-like glioblastoma cells via the MDM2-p53 axis. - Wikidata - awgldk - TriplyDB

MEK-ERK signaling dictates DNA-repair gene MGMT expression and temozolomide resistance of stem-like glioblastoma cells via the MDM2-p53 axis.

MEK-ERK signaling dictates DNA-repair gene MGMT expression and temozolomide resistance of stem-like glioblastoma cells via the MDM2-p53 axis.

http://www.wikidata.org/entity/Q48873373

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Understanding glioma stem cells: rationale, clinical relevance and therapeutic strategies Emerging Non-Canonical Functions and Regulation by p53: p53 and Stemness Data Mining Approaches for Genomic Biomarker Development: Applications Using Drug Screening Data from the Cancer Genome Project and the Cancer Cell Line Encyclopedia MEK2 is a prognostic marker and potential chemo-sensitizing target for glioma patients undergoing temozolomide treatment.A nanoparticle carrying the p53 gene targets tumors including cancer stem cells, sensitizes glioblastoma to chemotherapy and improves survival.Activity of temozolomide in patients with advanced chemorefractory colorectal cancer and MGMT promoter methylation.Ependymoma stem cells are highly sensitive to temozolomide in vitro and in orthotopic models.Wnt activation promotes neuronal differentiation of glioblastoma Molecular targeting of TRF2 suppresses the growth and tumorigenesis of glioblastoma stem cells.Role of MGMT as biomarker in colorectal cancer.Induction of the unfolded protein response drives enhanced metabolism and chemoresistance in glioma cells Combined inhibition of AKT/mTOR and MDM2 enhances Glioblastoma Multiforme cell apoptosis and differentiation of cancer stem cells.Disruption of NF-κB signaling by fluoxetine attenuates MGMT expression in glioma cells.Targeting JNK for therapeutic depletion of stem-like glioblastoma cells Heterogeneity of Cancer Stem Cells: Rationale for Targeting the Stem Cell Niche.Lower MGMT expression predicts better prognosis in proneural-like glioblastoma Glioma-initiating cell elimination by metformin activation of FOXO3 via AMPK.Network Modeling Identifies Patient-specific Pathways in Glioblastoma.Glioblastoma multiforme therapy and mechanisms of resistance.p53, a potential predictor of Helicobacter pylori infection-associated gastric carcinogenesis?Hepatitis B virus X protein promotes the stem-like properties of OV6+ cancer cells in hepatocellular carcinoma.Glioblastoma: molecular pathways, stem cells and therapeutic targets.Novel KDM1A inhibitors induce differentiation and apoptosis of glioma stem cells via unfolded protein response pathway.Regulation of cancer stem cells by RING finger ubiquitin ligases.Phosphoprotein analysis reveals MEK inhibition as a way to target non-small cell lung cancer tumor initiating cells.Bortezomib overcomes MGMT-related resistance of glioblastoma cell lines to temozolomide in a schedule-dependent manner.miR-181b modulates glioma cell sensitivity to temozolomide by targeting MEK1.Bortezomib downregulates MGMT expression in T98G glioblastoma cells.Dose-Dense Temozolomide in Patients with MGMT-Silenced Chemorefractory Colorectal Cancer.An overview of therapeutic approaches to brain tumor stem cells A Rationale for Targeting Extracellular Regulated Kinases ERK1 and ERK2 in Glioblastoma.Persistence of DNA adducts, hypermutation and acquisition of cellular resistance to alkylating agents in glioblastoma.Glycosylated extracellular vesicles released by glioblastoma cells are decorated by CCL18 allowing for cellular uptake via chemokine receptor CCR8.microRNA expression pattern modulates temozolomide response in GBM tumors with cancer stem cells.miR-204 reverses temozolomide resistance and inhibits cancer initiating cells phenotypes by degrading FAP-α in glioblastoma.Alterations in Cell Motility, Proliferation, and Metabolism in Novel Models of Acquired Temozolomide Resistant Glioblastoma.Investigating the role of Hedgehog/GLI1 signaling in glioblastoma cell response to temozolomide.Potential Strategies Overcoming the Temozolomide Resistance for Glioblastoma Re-expression of the p53 Gene by Inhibiting the Mdm-2 Receptor in Wild-type p53 Tumors for the Treatment of Glioblastoma: A Mini Review Apatinib suppresses cell growth and metastasis and promotes antitumor activity of temozolomide in glioma

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MEK-ERK signaling dictates DNA-repair gene MGMT expression and temozolomide resistance of stem-like glioblastoma cells via the MDM2-p53 axis.

http://www.wikidata.org/entity/Q48873373

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2011 nî lūn-bûn

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MEK-ERK signaling dictates DNA ...... a cells via the MDM2-p53 axis.

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MEK-ERK signaling dictates DNA ...... a cells via the MDM2-p53 axis.

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MEK-ERK signaling dictates DNA ...... a cells via the MDM2-p53 axis.

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MEK-ERK signaling dictates DNA ...... a cells via the MDM2-p53 axis.

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MEK-ERK signaling dictates DNA ...... a cells via the MDM2-p53 axis.

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Chifumi Kitanaka

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Eriko Watanabe

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Ken-ichiro Matsuda

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P2860

O6-Methylguanine DNA methyltransferase protein expression in tumor cells predicts outcome of temozolomide therapy in glioblastoma patients

Small-molecule inhibitors of the MDM2-p53 protein-protein interaction to reactivate p53 function: a novel approach for cancer therapy

Comprehensive genomic characterization defines human glioblastoma genes and core pathways

p53 is involved in regulation of the DNA repair gene O6-methylguanine-DNA methyltransferase (MGMT) by DNA damaging agents

Analysis of gene expression and chemoresistance of CD133+ cancer stem cells in glioblastoma

Malignant gliomas in adults

Tumor stem cells derived from glioblastomas cultured in bFGF and EGF more closely mirror the phenotype and genotype of primary tumors than do serum-cultured cell lines

MGMT promoter hypermethylation is a frequent, early, and consistent event in astrocytoma progression, and not correlated with TP53 mutation.

Standard therapy for glioblastoma--a review of where we are.

Correlation of O6-methylguanine methyltransferase (MGMT) promoter methylation with clinical outcomes in glioblastoma and clinical strategies to modulate MGMT activity.

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