c-Met signaling induces a reprogramming network and supports the glioblastoma stem-like phenotype. - Wikidata - wikimedia - TriplyDB

c-Met signaling induces a reprogramming network and supports the glioblastoma stem-like phenotype.

c-Met signaling induces a reprogramming network and supports the glioblastoma stem-like phenotype.

http://www.wikidata.org/entity/Q35049178

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Cancer Stem Cell Hierarchy in Glioblastoma Multiforme Heterogeneity and targeting of pancreatic cancer stem cells Targeting the epithelial to mesenchymal transition in glioblastoma: the emerging role of MET signaling Mechanisms of evasive resistance to anti-VEGF therapy in glioblastoma Roles of c-Met and RON kinases in tumor progression and their potential as therapeutic targets Adaptation to antiangiogenic therapy in neurological tumors Effects of dual targeting of tumor cells and stroma in human glioblastoma xenografts with a tyrosine kinase inhibitor against c-MET and VEGFR2 Ggnbp2 Is Essential for Pregnancy Success via Regulation of Mouse Trophoblast Stem Cell Proliferation and Differentiation Registered report: Wnt activity defines colon cancer stem cells and is regulated by the microenvironment Overcoming therapeutic resistance in glioblastoma: the way forward Multiple receptor tyrosine kinases converge on microRNA-134 to control KRAS, STAT5B, and glioblastoma Hepatocyte growth factor sensitizes brain tumors to c-MET kinase inhibition.Cancer stem cell heterogeneity: origin and new perspectives on CSC targeting The evolving landscape of glioblastoma stem cells.HIF1α regulates single differentiated glioma cell dedifferentiation to stem-like cell phenotypes with high tumorigenic potential under hypoxia Lipid metabolism enzyme ACSVL3 supports glioblastoma stem cell maintenance and tumorigenicity HMMR maintains the stemness and tumorigenicity of glioblastoma stem-like cells.Hsa-miR-574-5p negatively regulates MACC-1 expression to suppress colorectal cancer liver metastasis.c-Met signaling in the development of tumorigenesis and chemoresistance: potential applications in pancreatic cancer DNA double-strand breaks cooperate with loss of Ink4 and Arf tumor suppressors to generate glioblastomas with frequent Met amplification.Crosstalk between nuclear MET and SOX9/β-catenin correlates with castration-resistant prostate cancer A minimal connected network of transcription factors regulated in human tumors and its application to the quest for universal cancer biomarkers RNA-seq of 272 gliomas revealed a novel, recurrent PTPRZ1-MET fusion transcript in secondary glioblastomas.Kruppel-like factor-9 (KLF9) inhibits glioblastoma stemness through global transcription repression and integrin α6 inhibition.Ionizing radiations sustain glioblastoma cell dedifferentiation to a stem-like phenotype through survivin: possible involvement in radioresistance.Glial progenitors as targets for transformation in glioma.Single cell-derived clonal analysis of human glioblastoma links functional and genomic heterogeneity.GD3 synthase regulates epithelial-mesenchymal transition and metastasis in breast cancer.A leak pathway for luminal protons in endosomes drives oncogenic signalling in glioblastoma Induction of tumor initiation is dependent on CD44s in c-Met⁺ hepatocellular carcinoma Inhibition of mesothelioma cancer stem-like cells with adenovirus-mediated NK4 gene therapy.The hepatocyte growth factor receptor as a potential therapeutic target for dedifferentiated liposarcoma uPAR and cathepsin B inhibition enhanced radiation-induced apoptosis in gliomainitiating cells.Platelet-derived growth factor receptors differentially inform intertumoral and intratumoral heterogeneity Susceptibility of pancreatic cancer stem cells to reprogramming.Identification of Global DNA Methylation Signatures in Glioblastoma-Derived Cancer Stem Cells.CD133+ melanoma subpopulations contribute to perivascular niche morphogenesis and tumorigenicity through vasculogenic mimicry.The implications of cancer stem cells for cancer therapy.Wnt/β-catenin signaling is a key downstream mediator of MET signaling in glioblastoma stem cells.Biological and clinical implications of cancer stem cells in primary brain tumors.

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P2860

c-Met signaling induces a reprogramming network and supports the glioblastoma stem-like phenotype.

http://www.wikidata.org/entity/Q35049178

description

2011 nî lūn-bûn

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2011 թուականի Մայիսին հրատարակուած գիտական յօդուած

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2011 թվականի մայիսին 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

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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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c-Met signaling induces a repr ...... oblastoma stem-like phenotype.

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c-Met signaling induces a repr ...... oblastoma stem-like phenotype.

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c-Met signaling induces a repr ...... oblastoma stem-like phenotype.

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

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c-Met signaling induces a repr ...... ioblastoma stem-like phenotype

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P2093

Angela Li

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Bachchu Lal

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Bjorn Scheffler

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Daniel Trageser

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John Laterra

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Martin Glas

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Mingyao Ying

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Shuli Xia

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Yingying Sang

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Yunqing Li

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P2860

The epithelial-mesenchymal transition generates cells with properties of stem cells

Glioma stem cells promote radioresistance by preferential activation of the DNA damage response

Induction of pluripotent stem cells from mouse embryonic and adult fibroblast cultures by defined factors

Met, metastasis, motility and more

SSEA-1 is an enrichment marker for tumor-initiating cells in human glioblastoma

Isolation and characterization of tumorigenic, stem-like neural precursors from human glioblastoma

Linking the p53 tumour suppressor pathway to somatic cell reprogramming

Suppression of induced pluripotent stem cell generation by the p53-p21 pathway

c-Myc is required for maintenance of glioma cancer stem cells.

Defined factors induce reprogramming of gastrointestinal cancer cells

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9951-9956

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10.1073/PNAS.1016912108

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24

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108

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Alfredo Quinones-Hinojosa

Hugo Guerrero-Cazares

Charles G Eberhart

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2011-05-31T00:00:00Z

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51180384

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21628563

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