FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2415730918> ?p ?o ?g. }

• W2415730918 abstract "The past 40 years of research greatly transformed our understanding of breast cancer disease. The results of basic scientific findings were successfully translated into the development of therapeutic agents. Although enormous progress has been made, many important questions still remain.Developing specific inhibitors targeting cellular epigenetic program becomes one of the most active areas of current drug discovery efforts. Many new epigenetic enzymes become drug targets for cancer intervention.The work presented here was focused towards understanding the role of KDM5s and EZH2 epigenetic enzymes in breast cancer as potential targets for breast cancer intervention. These enzymes are known to regulate histone H3 lysine 4 and 27 trimethylation states, which largely affect genome wide transcriptional programs. Our preliminary studies have identified breast cancer patient groups whose survival outcome correlated with expression of KDM5s and EZH2 bound genes and respective H3K4me3 and H3K27me3 gene loci. In order to link deregulation of KDM5 and EZH2 proteins to breast cancer development, we looked for the evidence of correlation between the expressions level of KDM5s and EZH2 and breast cancer disease aggressiveness. This data informs development of strategies reducing expression levels of these enzymes as well as targeting their enzymatic activity. To test the effects of reduced expression level on breast cancer cell growth, we generated knock down of KDM5s and EZH2 in a variety of cancer cell lines and compared it to non-transformed mammary epithelial cells. By performing a variety of cell culture-based assays as well as conducting gene expression studies, we next aimed at the identification of cancer cell characteristics controlled by these epigenetic enzymes. Decrease in expression of these enzymes resulted in less aggressive cancer phenotype affecting cell proliferation, invasion, migration and survival. We further investigated the potency of selective EZH2 inhibitors on reducing breast cancer cell growth. Based on these results, we applied CRISPR-Cas9 genome engineering system to generate a breast cancer genome encoding catalytically inactive forms of KDM5s and EZH2. This novel epigenetic cancer model enables studies into causal role of epigenetic activities in breast cancer tumorigenesis, which will move our outstanding of cancer epigenetic mechanisms beyond incremental knowledge." @default.
• W2415730918 created "2016-06-24" @default.
• W2415730918 creator A5001981584 @default.
• W2415730918 date "2016-02-17" @default.
• W2415730918 modified "2023-09-27" @default.
• W2415730918 title "Investigating The Role Of Epigenetic Enzymes In Breast Cancer" @default.
• W2415730918 hasPublicationYear "2016" @default.
• W2415730918 type Work @default.
• W2415730918 sameAs 2415730918 @default.
• W2415730918 citedByCount "0" @default.
• W2415730918 crossrefType "dissertation" @default.
• W2415730918 hasAuthorship W2415730918A5001981584 @default.
• W2415730918 hasConcept C101762097 @default.
• W2415730918 hasConcept C104317684 @default.
• W2415730918 hasConcept C121608353 @default.
• W2415730918 hasConcept C150194340 @default.
• W2415730918 hasConcept C2780914512 @default.
• W2415730918 hasConcept C41091548 @default.
• W2415730918 hasConcept C50171091 @default.
• W2415730918 hasConcept C502942594 @default.
• W2415730918 hasConcept C530470458 @default.
• W2415730918 hasConcept C54355233 @default.
• W2415730918 hasConcept C86803240 @default.
• W2415730918 hasConceptScore W2415730918C101762097 @default.
• W2415730918 hasConceptScore W2415730918C104317684 @default.
• W2415730918 hasConceptScore W2415730918C121608353 @default.
• W2415730918 hasConceptScore W2415730918C150194340 @default.
• W2415730918 hasConceptScore W2415730918C2780914512 @default.
• W2415730918 hasConceptScore W2415730918C41091548 @default.
• W2415730918 hasConceptScore W2415730918C50171091 @default.
• W2415730918 hasConceptScore W2415730918C502942594 @default.
• W2415730918 hasConceptScore W2415730918C530470458 @default.
• W2415730918 hasConceptScore W2415730918C54355233 @default.
• W2415730918 hasConceptScore W2415730918C86803240 @default.
• W2415730918 hasLocation W24157309181 @default.
• W2415730918 hasOpenAccess W2415730918 @default.
• W2415730918 hasPrimaryLocation W24157309181 @default.
• W2415730918 hasRelatedWork W1560088051 @default.
• W2415730918 hasRelatedWork W1986552462 @default.
• W2415730918 hasRelatedWork W2025254126 @default.
• W2415730918 hasRelatedWork W2035411102 @default.
• W2415730918 hasRelatedWork W2052624043 @default.
• W2415730918 hasRelatedWork W2063336743 @default.
• W2415730918 hasRelatedWork W2126315841 @default.
• W2415730918 hasRelatedWork W2126941107 @default.
• W2415730918 hasRelatedWork W2146143823 @default.
• W2415730918 hasRelatedWork W2203393012 @default.
• W2415730918 hasRelatedWork W2406587956 @default.
• W2415730918 hasRelatedWork W2468262431 @default.
• W2415730918 hasRelatedWork W2549361759 @default.
• W2415730918 hasRelatedWork W2564767498 @default.
• W2415730918 hasRelatedWork W2779658312 @default.
• W2415730918 hasRelatedWork W2979386890 @default.
• W2415730918 hasRelatedWork W3088976686 @default.
• W2415730918 hasRelatedWork W3093775294 @default.
• W2415730918 hasRelatedWork W3205814058 @default.
• W2415730918 hasRelatedWork W371191881 @default.
• W2415730918 isParatext "false" @default.
• W2415730918 isRetracted "false" @default.
• W2415730918 magId "2415730918" @default.
• W2415730918 workType "dissertation" @default.