Lunatic fringe deficiency cooperates with the Met/Caveolin gene amplicon to induce basal-like breast cancer. - Wikidata - wikimedia - TriplyDB

Lunatic fringe deficiency cooperates with the Met/Caveolin gene amplicon to induce basal-like breast cancer.

Lunatic fringe deficiency cooperates with the Met/Caveolin gene amplicon to induce basal-like breast cancer.

http://www.wikidata.org/entity/Q36702175

about

The notch ligand JAGGED1 as a target for anti-tumor therapy A Role for Notch Signalling in Breast Cancer and Endocrine Resistance From fly wings to targeted cancer therapies: a centennial for notch signaling Manic fringe inhibits tumor growth by suppressing Notch3 degradation in lung cancer Targeting Met and Notch in the Lfng-deficient, Met-amplified triple-negative breast cancer.NOTCH1 inhibition in vivo results in mammary tumor regression and reduced mammary tumorsphere-forming activity in vitro Weight Loss Reversed Obesity-Induced HGF/c-Met Pathway and Basal-Like Breast Cancer Progression Notch and TGFβ: Functional partners facilitating tumor progression Notch inhibitors for cancer treatment.Profiling the tyrosine phosphoproteome of different mouse mammary tumour models reveals distinct, model-specific signalling networks and conserved oncogenic pathways.Manic fringe promotes a claudin-low breast cancer phenotype through notch-mediated PIK3CG induction.Cross-species DNA copy number analyses identifies multiple 1q21-q23 subtype-specific driver genes for breast cancer Jagged mediates differences in normal and tumor angiogenesis by affecting tip-stalk fate decision.p53 Modulates Notch Signaling in MCF-7 Breast Cancer Cells by Associating With the Notch Transcriptional Complex Via MAML1 Breast cancer regulated by Fringe.Lunatic, Manic, and Radical Fringe Each Promote T and B Cell Development Molecular characterization of basal-like and non-basal-like triple-negative breast cancer.Met synergizes with p53 loss to induce mammary tumors that possess features of claudin-low breast cancer.Correlation of Notch1, pAKT and nuclear NF-κB expression in triple negative breast cancer.Genomic profiling of murine mammary tumors identifies potential personalized drug targets for p53-deficient mammary cancers.A Tumor initiating cell-enriched prognostic signature for HER2+:ERα- breast cancer; rationale, new features, controversies and future directions Notch3 marks clonogenic mammary luminal progenitor cells in vivo.Role of HGF in obesity-associated tumorigenesis: C3(1)-TAg mice as a model for human basal-like breast cancer.Prolyl-isomerase Pin1 controls normal and cancer stem cells of the breast.Tumor-suppressive activity of Lunatic Fringe in prostate through differential modulation of Notch receptor activation.Pygopus 2: tilting the Wnt-Notch balance in mammary epithelial lineage determination Tumor-infiltrating myeloid cells activate Dll4/Notch/TGF-β signaling to drive malignant progression Significance of glycosylation in Notch signaling.Ran GTPase promotes cancer progression via Met recepto-rmediated downstream signaling.Identification of the microRNA expression profile in the regenerative neonatal mouse heart by deep sequencing.Low-grade and high-grade mammary carcinomas in WAP-T transgenic mice are independent entities distinguished by Met expression.Deciphering the Fringe-Mediated Notch Code: Identification of Activating and Inhibiting Sites Allowing Discrimination between Ligands.Lunatic fringe-mediated Notch signaling regulates adult hippocampal neural stem cell maintenance.Notch system is differentially expressed and activated in pituitary adenomas of distinct histotype, tumor cell lines and normal pituitaries Whole-exome DNA sequence analysis of Brca2- and Trp53-deficient mouse mammary gland tumours.Lunatic Fringe and p53 Cooperatively Suppress Mesenchymal Stem-Like Breast Cancer.Stromal PTEN inhibits the expansion of mammary epithelial stem cells through Jagged-1 KrasG12D upregulates Notch signaling to induce gallbladder tumorigenesis in mice.Comparative genomics reveals that loss of lunatic fringe (LFNG) promotes melanoma metastasis.Numb prevents a complete epithelial-mesenchymal transition by modulating Notch signalling.

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P2860

Lunatic fringe deficiency cooperates with the Met/Caveolin gene amplicon to induce basal-like breast cancer.

http://www.wikidata.org/entity/Q36702175

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Lunatic fringe deficiency coop ...... duce basal-like breast cancer.

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Lunatic fringe deficiency coop ...... duce basal-like breast cancer.

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Lunatic fringe deficiency coop ...... duce basal-like breast cancer.

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Lunatic fringe deficiency coop ...... duce basal-like breast cancer.

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Lunatic fringe deficiency coop ...... duce basal-like breast cancer.

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Lunatic fringe deficiency coop ...... duce basal-like breast cancer.

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J.CCR.2012.03.041

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Lunatic fringe deficiency coop ...... nduce basal-like breast cancer

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Amanda J Loch

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Cynthia J Guidos

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Dong-Yu Wang

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Eldad Zacksenhaus

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Jerry Usary

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Jessica R Adams

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Joseph Beyene

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Keli Xu

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Nicholas Gaiano

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Philaretos C Kousis

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P2860

Activation of multiple proto-oncogenic tyrosine kinases in breast cancer via loss of the PTPN12 phosphatase

Jagged1-mediated Notch activation induces epithelial-to-mesenchymal transition through Slug-induced repression of E-cadherin.

A family of mammalian Fringe genes implicated in boundary determination and the Notch pathway

Cooperative epigenetic modulation by cancer amplicon genes

ALDH1 is a marker of normal and malignant human mammary stem cells and a predictor of poor clinical outcome

IL-6 triggers malignant features in mammospheres from human ductal breast carcinoma and normal mammary gland

Loss of negative regulation by Numb over Notch is relevant to human breast carcinogenesis

Fringe boundaries coincide with Notch-dependent patterning centres in mammals and alter Notch-dependent development in Drosophila

MMTV-induced mammary tumorigenesis: gene discovery, progression to malignancy and cellular pathways

Basal-like breast cancer defined by five biomarkers has superior prognostic value than triple-negative phenotype

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626-641

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21

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Charles M. Perou

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