scholarly journals Integrative analysis of genome-wide loss of heterozygosity and monoallelic expression at nucleotide resolution reveals disrupted pathways in triple-negative breast cancer

2012 ◽  
Vol 22 (10) ◽  
pp. 1995-2007 ◽  
Author(s):  
G. Ha ◽  
A. Roth ◽  
D. Lai ◽  
A. Bashashati ◽  
J. Ding ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Loss Of Heterozygosity ◽  
Triple Negative Breast Cancer ◽  
Triple Negative ◽  
Integrative Analysis ◽  
Monoallelic Expression ◽  
Genome Wide ◽  
Nucleotide Resolution

scholarly journals A Genome-wide siRNA Screen Identifies Proteasome Addiction as a Vulnerability of Basal-like Triple-Negative Breast Cancer Cells

Cancer Cell ◽  
2013 ◽  
Vol 24 (2) ◽  
pp. 182-196 ◽  
Author(s):  
Fabio Petrocca ◽  
Gabriel Altschuler ◽  
Shen Mynn Tan ◽  
Marc L. Mendillo ◽  
Haoheng Yan ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Triple Negative Breast Cancer ◽  
Breast Cancer Cells ◽  
Triple Negative ◽  
Sirna Screen ◽  
Genome Wide ◽  
A Genome

scholarly journals Integrative analysis of lncRNAs and miRNAs with coding RNAs associated with ceRNA crosstalk network in triple negative breast cancer

2017 ◽  
Vol Volume 10 ◽  
pp. 5883-5897 ◽  
Author(s):  
Naijun Yuan ◽  
Guijuan Zhang ◽  
Fengjie Bie ◽  
Min Ma ◽  
Yi Ma ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Triple Negative Breast Cancer ◽  
Triple Negative ◽  
Integrative Analysis

scholarly journals A Review of the Hereditary Component of Triple Negative Breast Cancer: High- and Moderate-Penetrance Breast Cancer Genes, Low-Penetrance Loci, and the Role of Nontraditional Genetic Elements

2019 ◽  
Vol 2019 ◽  
pp. 1-10 ◽  
Author(s):  
Darrell L. Ellsworth ◽  
Clesson E. Turner ◽  
Rachel E. Ellsworth
Keyword(s):  
Breast Cancer ◽  
Triple Negative Breast Cancer ◽  
Large Scale ◽  
Triple Negative ◽  
Association Studies ◽  
African Ancestry ◽  
Genome Wide Association Studies ◽  
Genetic Elements ◽  
Genome Wide ◽  
Increased Risk

Triple negative breast cancer (TNBC), representing 10-15% of breast tumors diagnosed each year, is a clinically defined subtype of breast cancer associated with poor prognosis. The higher incidence of TNBC in certain populations such as young women and/or women of African ancestry and a unique pathological phenotype shared between TNBC and BRCA1-deficient tumors suggest that TNBC may be inherited through germline mutations. In this article, we describe genes and genetic elements, beyond BRCA1 and BRCA2, which have been associated with increased risk of TNBC. Multigene panel testing has identified high- and moderate-penetrance cancer predisposition genes associated with increased risk for TNBC. Development of large-scale genome-wide SNP assays coupled with genome-wide association studies (GWAS) has led to the discovery of low-penetrance TNBC-associated loci. Next-generation sequencing has identified variants in noncoding RNAs, viral integration sites, and genes in underexplored regions of the human genome that may contribute to the genetic underpinnings of TNBC. Advances in our understanding of the genetics of TNBC are driving improvements in risk assessment and patient management.

scholarly journals Hyperinsulinemia promotes aberrant histone acetylation in triple negative breast cancer

2018 ◽  
Author(s):  
Parijat Senapati ◽  
Christine Thai ◽  
Angelica Sanchez ◽  
Emily J Gallagher ◽  
Derek LeRoith ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Histone Acetylation ◽  
Triple Negative Breast Cancer ◽  
Triple Negative ◽  
Prognostic Indicator ◽  
Gene Promoters ◽  
Genome Wide ◽  
Altered Gene ◽  
The Impact

AbstractExcess levels of insulin relative to glucose in the blood, or hyperinsulinemia, is considered to be a poor prognostic indicator for patients with triple negative breast cancer (TNBC). While this association has been recognized for some time, the mechanistic role of hyperinsulinemia in promoting TNBC remains unclear. We show that insulin treatment leads to genome-wide increase in histone acetylation, in particular at H3K9, through the PI3K/AKT/mTOR pathway in MDA-MB-231 cells. Genome-wide analysis showed that the increase in histone acetylation occurs primarily at gene promoters. In addition, insulin induces higher levels of reactive oxygen species and DNA damage foci in cells. In vivo, hyperinsulinemia also enhances growth of MDA-MB-231 derived tumors through increased histone acetylation. These results demonstrate the impact of hyperinsulinemia on altered gene regulation through chromatin and the importance of targeting hyperinsulinemia-induced processes that lead to chromatin dysfunction in TNBC.

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