Identification and functional analysis of 9p24 amplified genes in human breast cancer. - Wikidata - awgldk - TriplyDB

Identification and functional analysis of 9p24 amplified genes in human breast cancer.

Identification and functional analysis of 9p24 amplified genes in human breast cancer.

http://www.wikidata.org/entity/Q34191958

about

NIRF/UHRF2 occupies a central position in the cell cycle network and allows coupling with the epigenetic landscape KDM4C and ATF4 Cooperate in Transcriptional Control of Amino Acid Metabolism A community effort to assess and improve drug sensitivity prediction algorithms.The Discovery of Novel Biomarkers Improves Breast Cancer Intrinsic Subtype Prediction and Reconciles the Labels in the METABRIC Data Set.Interplay between epigenetics and metabolism in oncogenesis: mechanisms and therapeutic approaches A polymorphism in JMJD2C alters the cleavage by caspase-3 and the prognosis of human breast cancer.UTX and MLL4 coordinately regulate transcriptional programs for cell proliferation and invasiveness in breast cancer cells.Histone demethylase GASC1--a potential prognostic and predictive marker in invasive breast cancer.Genomic amplification and a role in drug-resistance for the KDM5A histone demethylase in breast cancer Genomic amplification of 9p24.1 targeting JAK2, PD-L1, and PD-L2 is enriched in high-risk triple negative breast cancer.Histone demethylase JMJD2C is a coactivator for hypoxia-inducible factor 1 that is required for breast cancer progression.An integrated genomic analysis of Tudor domain-containing proteins identifies PHD finger protein 20-like 1 (PHF20L1) as a candidate oncogene in breast cancer C14orf166 overexpression correlates with tumor progression and poor prognosis of breast cancer UHRF2, a ubiquitin E3 ligase, acts as a small ubiquitin-like modifier E3 ligase for zinc finger protein 131.Multidimensional Proteomics Reveals a Role of UHRF2 in the Regulation of Epithelial-Mesenchymal Transition (EMT).Identification of Copy Number Aberrations in Breast Cancer Subtypes Using Persistence Topology.Genome-wide identification of genes with amplification and/or fusion in small cell lung cancer Histone demethylase GASC1, a potential prognostic and predictive marker in esophageal squamous cell carcinoma.KDM4C Activity Modulates Cell Proliferation and Chromosome Segregation in Triple-Negative Breast Cancer.Identification of IL11RA and MELK amplification in gastric cancer by comprehensive genomic profiling of gastric cancer cell lines.Triple-negative breast cancers with amplification of JAK2 at the 9p24 locus demonstrate JAK2-specific dependence.ERMP1, a novel potential oncogene involved in UPR and oxidative stress defense, is highly expressed in human cancer Histone lysine demethylase (KDM) subfamily 4: structures, functions and therapeutic potential.Recurring DNA copy number gain at chromosome 9p13 plays a role in the activation of multiple candidate oncogenes in progressing oral premalignant lesions.Reactivation of multipotency by oncogenic PIK3CA induces breast tumour heterogeneity.UHRF2 decreases H3K9ac expression by interacting with it through the PHD and SRA/YDG domain in HepG2 hepatocellular carcinoma cells.Post-Transcriptional Regulation of the GASC1 Oncogene with Active Tumor-Targeted siRNA-Nanoparticles.Epigenetic control and cancer: the potential of histone demethylases as therapeutic targets.Copy number alterations and neoplasia-specific mutations in MELK, PDCD1LG2, TLN1, and PAX5 at 9p in different neoplasias.Histone demethylase JMJD2C: epigenetic regulators in tumors.Overexpression of UHRF2 in intrahepatic cholangiocarcinoma and its clinical significance.Investigational PD-1 inhibitors in HL and NHL and biomarkers for predictors of response and outcome.Development and validation of a novel clinical fluorescence in situ hybridization assay to detect JAK2 and PD-L1 amplification: a fluorescence in situ hybridization assay for JAK2 and PD-L1 amplification.Pan-cancer analysis of copy number changes in programmed death-ligand 1 (PD-L1, CD274) - associations with gene expression, mutational load, and survival.

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Identification and functional analysis of 9p24 amplified genes in human breast cancer.

http://www.wikidata.org/entity/Q34191958

description

2011 nî lūn-bûn

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2011 թուականի Յունիսին հրատարակուած գիտական յօդուած

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2011 թվականի հունիսին հրատարակված գիտական հոդված

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2011年の論文

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2011年学术文章

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2011年学术文章

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2011年学术文章

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2011年學術文章

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name

Identification and functional analysis of 9p24 amplified genes in human breast cancer.

@ast

Identification and functional analysis of 9p24 amplified genes in human breast cancer.

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Identification and functional analysis of 9p24 amplified genes in human breast cancer.

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type

label

Identification and functional analysis of 9p24 amplified genes in human breast cancer.

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Identification and functional analysis of 9p24 amplified genes in human breast cancer.

@en

Identification and functional analysis of 9p24 amplified genes in human breast cancer.

@nl

prefLabel

Identification and functional analysis of 9p24 amplified genes in human breast cancer.

@ast

Identification and functional analysis of 9p24 amplified genes in human breast cancer.

@en

Identification and functional analysis of 9p24 amplified genes in human breast cancer.

@nl

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Identification and functional analysis of 9p24 amplified genes in human breast cancer.

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A Dombkowski

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G Liu

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J Abrams

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J Wu

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M S Wicha

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P2860

NIRF, a novel RING finger protein, is involved in cell-cycle regulation

Reversal of histone lysine trimethylation by the JMJD2 family of histone demethylases

Cooperative epigenetic modulation by cancer amplicon genes

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

Rapid colorimetric assay for cellular growth and survival: Application to proliferation and cytotoxicity assays

Structure and Hemimethylated CpG Binding of the SRA Domain from Human UHRF1

The consensus coding sequences of human breast and colorectal cancers

WAF1, a potential mediator of p53 tumor suppression

Histone demethylation by a family of JmjC domain-containing proteins.

The tyrosine phosphatase PTPRD is a tumor suppressor that is frequently inactivated and mutated in glioblastoma and other human cancers

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