Maintenance of hormone responsiveness in luminal breast cancers by suppression of Notch - Wikidata - wikimedia - TriplyDB

Maintenance of hormone responsiveness in luminal breast cancers by suppression of Notch

Maintenance of hormone responsiveness in luminal breast cancers by suppression of Notch

http://www.wikidata.org/entity/Q35779391

about

The notch ligand JAGGED1 as a target for anti-tumor therapy A Role for Notch Signalling in Breast Cancer and Endocrine Resistance Steroid hormones, steroid receptors, and breast cancer stem cells Identifying and targeting tumor-initiating cells in the treatment of breast cancer Γ-secretase components as predictors of breast cancer outcome Genome-wide profiles of methylation, microRNAs, and gene expression in chemoresistant breast cancer Notch and Mef2 synergize to promote proliferation and metastasis through JNK signal activation in Drosophila Prognostic value of gene signatures and proliferation in lymph-node-negative breast cancer Keratin 5 overexpression is associated with serous ovarian cancer recurrence and chemotherapy resistance.Aurora-A mitotic kinase induces endocrine resistance through down-regulation of ERα expression in initially ERα+ breast cancer cells.High fat diet alters lactation outcomes: possible involvement of inflammatory and serotonergic pathways.Modeling luminal breast cancer heterogeneity: combination therapy to suppress a hormone receptor-negative, cytokeratin 5-positive subpopulation in luminal disease.The functional interaction between Acyl-CoA synthetase 4, 5-lipooxygenase and cyclooxygenase-2 controls tumor growth: a novel therapeutic target.Differential regulation of breast cancer-associated genes by progesterone receptor isoforms PRA and PRB in a new bi-inducible breast cancer cell line.Progestin suppression of miR-29 potentiates dedifferentiation of breast cancer cells via KLF4.FOXC1 is a critical mediator of EGFR function in human basal-like breast cancer.New targeted therapies for breast cancer: A focus on tumor microenvironmental signals and chemoresistant breast cancers Luminal breast cancer metastases and tumor arousal from dormancy are promoted by direct actions of estradiol and progesterone on the malignant cells Progress in breast cancer research.c-Jun N-terminal kinase 2 prevents luminal cell commitment in normal mammary glands and tumors by inhibiting p53/Notch1 and breast cancer gene 1 expression.Regulators of genetic risk of breast cancer identified by integrative network analysis.Mesenchymal traits are selected along with stem features in breast cancer cells grown as mammospheres.Progesterone-inducible cytokeratin 5-positive cells in luminal breast cancer exhibit progenitor properties.ER, PR, HER2, Ki-67 and CK5 in Early and Late Relapsing Breast Cancer-Reduced CK5 Expression in Metastases.Lunatic fringe deficiency cooperates with the Met/Caveolin gene amplicon to induce basal-like breast cancer.Steroid induction of therapy-resistant cytokeratin-5-positive cells in estrogen receptor-positive breast cancer through a BCL6-dependent mechanism.Correlation of Notch1, pAKT and nuclear NF-κB expression in triple negative breast cancer.Genome-wide reprogramming of the chromatin landscape underlies endocrine therapy resistance in breast cancer.Oestrogen increases the activity of oestrogen receptor negative breast cancer stem cells through paracrine EGFR and Notch signalling.Crosstalk between PKCα and Notch-4 in endocrine-resistant breast cancer cells.BRCA1 is a key regulator of breast differentiation through activation of Notch signalling with implications for anti-endocrine treatment of breast cancers.Patient-derived luminal breast cancer xenografts retain hormone receptor heterogeneity and help define unique estrogen-dependent gene signatures.Prolactin suppresses a progestin-induced CK5-positive cell population in luminal breast cancer through inhibition of progestin-driven BCL6 expression.EZH2 expands breast stem cells through activation of NOTCH1 signaling.Evidence for the existence of triple-negative variants in the MCF-7 breast cancer cell population.Competing endogenous RNA network analysis identifies critical genes among the different breast cancer subtypes.Drug resistance to targeted therapies: déjà vu all over again A New Role for ERα: Silencing via DNA Methylation of Basal, Stem Cell, and EMT Genes.High level PHGDH expression in breast is predominantly associated with keratin 5-positive cell lineage independently of malignancy.Combining Notch inhibition with current therapies for breast cancer treatment.

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Maintenance of hormone responsiveness in luminal breast cancers by suppression of Notch

http://www.wikidata.org/entity/Q35779391

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name

Maintenance of hormone responsiveness in luminal breast cancers by suppression of Notch

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Maintenance of hormone responsiveness in luminal breast cancers by suppression of Notch

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type

label

Maintenance of hormone responsiveness in luminal breast cancers by suppression of Notch

@ast

Maintenance of hormone responsiveness in luminal breast cancers by suppression of Notch

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prefLabel

Maintenance of hormone responsiveness in luminal breast cancers by suppression of Notch

@ast

Maintenance of hormone responsiveness in luminal breast cancers by suppression of Notch

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PNAS.1106509108

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

P1476

Maintenance of hormone responsiveness in luminal breast cancers by suppression of Notch

@en

P2093

Brian S Bliesner

http://www.w3.org/2001/XMLSchema#string

Carol A Sartorius

http://www.w3.org/2001/XMLSchema#string

James M Haughian

http://www.w3.org/2001/XMLSchema#string

Kathryn B Horwitz

http://www.w3.org/2001/XMLSchema#string

Kristiina M Joensuu

http://www.w3.org/2001/XMLSchema#string

Päivi Heikkilä

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Wendy W Dye

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P2860

Role of Notch signaling in cell-fate determination of human mammary stem/progenitor cells

A comparison of gene expression signatures from breast tumors and breast tissue derived cell lines

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

A collection of breast cancer cell lines for the study of functionally distinct cancer subtypes

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

Prospective identification of tumorigenic breast cancer cells

Human acute myeloid leukemia is organized as a hierarchy that originates from a primitive hematopoietic cell

Molecular portraits of human breast tumours

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

Phenotypic and molecular characterization of the claudin-low intrinsic subtype of breast cancer

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8

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109

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Charles M. Perou

Mauricio P Pinto

J Chuck Harrell

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2011-10-03T00:00:00Z

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51691252

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21969591

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3287001

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