MYC pathway activation in triple-negative breast cancer is synthetic lethal with CDK inhibition - Wikidata - awgldk - TriplyDB

MYC pathway activation in triple-negative breast cancer is synthetic lethal with CDK inhibition

MYC pathway activation in triple-negative breast cancer is synthetic lethal with CDK inhibition

http://www.wikidata.org/entity/Q35894198

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Regulation of Bim in Health and Disease Genomic profiling of small-cell lung cancer: the era of targeted therapies Coordination of nutrient availability and utilization by MAX- and MLX-centered transcription networks Identification of Chemical Inhibitors of β-Catenin-Driven Liver Tumorigenesis in Zebrafish CDK1 Is a Synthetic Lethal Target for KRAS Mutant Tumours.Cancer's Achilles' Heel: Apoptosis and Necroptosis to the Rescue A model of spontaneous mouse mammary tumor for human estrogen receptor- and progesterone receptor-negative breast cancer Inhibition of mTOR-kinase destabilizes MYCN and is a potential therapy for MYCN-dependent tumors Serum anti-MDM2 and anti-c-Myc autoantibodies as biomarkers in the early detection of lung cancer.Bayesian mixture models for assessment of gene differential behaviour and prediction of pCR through the integration of copy number and gene expression data.Meta-analysis of the global gene expression profile of triple-negative breast cancer identifies genes for the prognostication and treatment of aggressive breast cancer Stimuli-Responsive Mesoporous Silica NPs as Non-viral Dual siRNA/Chemotherapy Carriers for Triple Negative Breast Cancer.A c-Myc-regulated stem cell-like signature in high-risk neuroblastoma: A systematic discovery (Target neuroblastoma ESC-like signature).Suppressive role exerted by microRNA-29b-1-5p in triple negative breast cancer through SPIN1 regulation.Triple-negative breast cancer: challenges and opportunities of a heterogeneous disease.Oncogenic protein MTBP interacts with MYC to promote tumorigenesis CDK/CK1 inhibitors roscovitine and CR8 downregulate amplified MYCN in neuroblastoma cells.A pan-cancer proteomic perspective on The Cancer Genome Atlas.Lung adenocarcinoma subtypes based on expression of human airway basal cell genes MTBP is overexpressed in triple-negative breast cancer and contributes to its growth and survival.Myc is required for β-catenin-mediated mammary stem cell amplification and tumorigenesis.Wnt signaling blockage inhibits cell proliferation and migration, and induces apoptosis in triple-negative breast cancer cells.CDK7-dependent transcriptional addiction in triple-negative breast cancer.Wnt modulates MCL1 to control cell survival in triple negative breast cancer.Concordance of genomic alterations between primary and recurrent breast cancer.Linking tumor mutations to drug responses via a quantitative chemical-genetic interaction map.Mechanism of action and therapeutic efficacy of Aurora kinase B inhibition in MYC overexpressing medulloblastoma.Metabolic reprogramming in triple-negative breast cancer through Myc suppression of TXNIP Repression of SRF target genes is critical for Myc-dependent apoptosis of epithelial cells.Midostaurin preferentially attenuates proliferation of triple-negative breast cancer cell lines through inhibition of Aurora kinase family.An integrated bioinformatics analysis to dissect kinase dependency in triple negative breast cancer.MYC Is a Major Determinant of Mitotic Cell Fate.microRNA-206 impairs c-Myc-driven cancer in a synthetic lethal manner by directly inhibiting MAP3K13.Immunohistochemical, genetic and epigenetic profiles of hereditary and triple negative breast cancers. Relevance in personalized medicine Inferring synthetic lethal interactions from mutual exclusivity of genetic events in cancer.Single-cell analysis reveals a stem-cell program in human metastatic breast cancer cells A novel HMGA1-CCNE2-YAP axis regulates breast cancer aggressiveness.Molecular pathways: the metabolic regulator estrogen-related receptor α as a therapeutic target in cancer.Targeting Glutamine Metabolism in Breast Cancer with Aminooxyacetate.Targeting MYC in cancer therapy: RNA processing offers new opportunities.

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P2860

MYC pathway activation in triple-negative breast cancer is synthetic lethal with CDK inhibition

http://www.wikidata.org/entity/Q35894198

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2012 nî lūn-bûn

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2012年の論文

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2012年論文

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2012年論文

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2012年論文

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2012年論文

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2012年論文

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2012年论文

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2012年论文

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2012年论文

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name

MYC pathway activation in trip ...... tic lethal with CDK inhibition

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MYC pathway activation in trip ...... tic lethal with CDK inhibition

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type

label

MYC pathway activation in trip ...... tic lethal with CDK inhibition

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MYC pathway activation in trip ...... tic lethal with CDK inhibition

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prefLabel

MYC pathway activation in trip ...... tic lethal with CDK inhibition

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MYC pathway activation in trip ...... tic lethal with CDK inhibition

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Journal of Experimental Medicine

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MYC pathway activation in trip ...... tic lethal with CDK inhibition

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P2093

Alexey V Bazarov

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

Ana Maria Gonzalez-Angulo

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Andrei Goga

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Dai Horiuchi

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Gordon B Mills

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Katelyn J Creasman

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Laura J Esserman

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Leonard Kusdra

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Marc E Lenburg

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Noelle E Huskey

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P2860

Bim: a novel member of the Bcl-2 family that promotes apoptosis

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

Functional role and oncogene-regulated expression of the BH3-only factor Bmf in mammary epithelial anoikis and morphogenesis

Analysis of Relative Gene Expression Data Using Real-Time Quantitative PCR and the 2−ΔΔCT Method

Exploiting chemical libraries, structure, and genomics in the search for kinase inhibitors

Inhibition of poly(ADP-ribose) polymerase in tumors from BRCA mutation carriers.

Gene expression patterns of breast carcinomas distinguish tumor subclasses with clinical implications

Gene expression profiling predicts clinical outcome of breast cancer

Molecular portraits of human breast tumours

The Myc/Max/Mad network and the transcriptional control of cell behavior

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679-696

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10.1084/JEM.20111512

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209

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Sanjay Chandriani

James W P Smyth

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2012-03-19T00:00:00Z

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221723141

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22430491

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3328367

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