Functional Genomic Landscape of Human Breast Cancer Drivers, Vulnerabilities, and Resistance. - Wikidata - awgldk - TriplyDB

Functional Genomic Landscape of Human Breast Cancer Drivers, Vulnerabilities, and Resistance.

Functional Genomic Landscape of Human Breast Cancer Drivers, Vulnerabilities, and Resistance.

http://www.wikidata.org/entity/Q36496096

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Molecular biology of breast tumors and prognosis The Bromodomain and Extra-Terminal Domain (BET) Family: Functional Anatomy of BET Paralogous Proteins Two Distinct Types of E3 Ligases Work in Unison to Regulate Substrate Ubiquitylation A Biobank of Breast Cancer Explants with Preserved Intra-tumor Heterogeneity to Screen Anticancer Compounds Serotonergic system antagonists target breast tumor initiating cells and synergize with chemotherapy to shrink human breast tumor xenografts.Characterization of Human Cancer Cell Lines by Reverse-phase Protein Arrays Impact of outdated gene annotations on pathway enrichment analysis.g:Profiler-a web server for functional interpretation of gene lists (2016 update)PROTAC-induced BET protein degradation as a therapy for castration-resistant prostate cancer.Cbx8 Acts Non-canonically with Wdr5 to Promote Mammary Tumorigenesis.Loss of TRIM33 causes resistance to BET bromodomain inhibitors through MYC- and TGF-β-dependent mechanisms Plasma exosome microRNAs are indicative of breast cancer.Phospho-BRD4: transcription plasticity and drug targeting.Integrative exploration of genomic profiles for triple negative breast cancer identifies potential drug targets.Serotonin transporter antagonists target tumor-initiating cells in a transgenic mouse model of breast cancer.Targeting BET bromodomain proteins in solid tumors CX-5461 is a DNA G-quadruplex stabilizer with selective lethality in BRCA1/2 deficient tumours Improved anticancer drug response prediction in cell lines using matrix factorization with similarity regularization.Downregulation of BRD4 inhibits gallbladder cancer proliferation and metastasis and induces apoptosis via PI3K/AKT pathway.Seed-effect modeling improves the consistency of genome-wide loss-of-function screens and identifies synthetic lethal vulnerabilities in cancer cells.Defining a Cancer Dependency Map.Systematic Drug Screening Identifies Tractable Targeted Combination Therapies in Triple-Negative Breast Cancer.Bromodomain and Extraterminal Protein Inhibition Blocks Growth of Triple-negative Breast Cancers through the Suppression of Aurora Kinases.Copy-number and gene dependency analysis reveals partial copy loss of wild-type SF3B1 as a novel cancer vulnerability.BET Bromodomain Proteins as Cancer Therapeutic Targets.Transcriptome- and proteome-oriented identification of dysregulated eIF4G, STAT3, and Hippo pathways altered by PIK3CA H1047R in HER2/ER-positive breast cancer.Prostate-derived Ets factor, an oncogenic driver in breast cancer.Phytochemicals Targeting Estrogen Receptors: Beneficial Rather Than Adverse Effects?Network-Based Identification and Prioritization of Key Regulators of Coronary Artery Disease Loci.VGLL4 Selectively Represses YAP-Dependent Gene Induction and Tumorigenic Phenotypes in Breast Cancer CancerGD: A Resource for Identifying and Interpreting Genetic Dependencies in Cancer.CRISPR/Cas9 mutagenesis invalidates a putative cancer dependency targeted in on-going clinical trials.Genotranscriptomic meta-analysis of the CHD family chromatin remodelers in human cancers - initial evidence of an oncogenic role for CHD7.Resistance to BET Bromodomain Inhibitors Is Mediated by Kinome Reprogramming in Ovarian Cancer.Basal-A Triple Negative Breast Cancer Cells Selectively Rely on RNA Splicing for Survival.Gene isoforms as expression-based biomarkers predictive of drug response in vitro.A Community Challenge for Inferring Genetic Predictors of Gene Essentialities through Analysis of a Functional Screen of Cancer Cell Lines.The 26S proteasome: A cell cycle regulator regulated by cell cycle Targeted Degradation of BET Proteins in Triple-Negative Breast Cancer.A Compendium of Co-regulated Protein Complexes in Breast Cancer Reveals Collateral Loss Events.

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Functional Genomic Landscape of Human Breast Cancer Drivers, Vulnerabilities, and Resistance.

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Benjamin G Neel

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P2860

IL-32 synergizes with nucleotide oligomerization domain (NOD) 1 and NOD2 ligands for IL-1beta and IL-6 production through a caspase 1-dependent mechanism

Cancer vulnerabilities unveiled by genomic loss

Selective inhibition of BET bromodomains

Comprehensive molecular portraits of human breast tumours

FoxA1 translates epigenetic signatures into enhancer-driven lineage-specific transcription

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

CBP/p300 interact with and function as transcriptional coactivators of BRCA1

Integrated genomic analyses of ovarian carcinoma

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

Molecular portraits of human breast tumours

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