CIDR_Epidemiology of Breast Cancer Subtypes in African American Women
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PROVIDER: PRJNA222875 | ENA |
REPOSITORIES: ENA
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Project description:In the United States, African-American (AA) women are more likely to develop early-onset breast cancer and have historically poorer outcomes due to this disease compared to European-American (EA) women. Here, we analyzed genomic profiles of breast tumors from young women (<50 years old), matched by tumor subtype, histological grade, and ethnicity (African-American, AA, compared to European-American, EA). DNA copy number alterations (CNAs) were analyzed on the Affymetrix Human SNP Array v 6.0 platform. The study provides insight into the genetic component of ethnicity-related breast cancer health disparities.
2013-01-29 | GSE26232 | GEO
Project description:In the United States, African-American (AA) women are more likely to develop early-onset breast cancer and have historically poorer outcomes due to this disease compared to European-American (EA) women. Here, we analyzed genomic profiles of breast tumors from young women (<50 years old), matched by tumor subtype, histological grade, and ethnicity (African-American, AA, compared to European-American, EA). DNA copy number alterations (CNAs) were analyzed using a 32K BAC tiling path array. The study provides insight into the genetic component of ethnicity-related breast cancer health disparities.
2013-01-29 | GSE26214 | GEO
Project description:In the United States, African-American (AA) women are more likely to develop early-onset breast cancer and have historically poorer outcomes due to this disease compared to European-American (EA) women. Here, we analyzed genomic profiles of breast tumors from young women (<50 years old), matched by tumor subtype, histological grade, and ethnicity (African-American, AA, compared to European-American, EA). DNA copy number alterations (CNAs) were analyzed using a 32K BAC tiling path array. The study provides insight into the genetic component of ethnicity-related breast cancer health disparities. Breast tumor samples from young women (< 50 years old) were matched as follows: a matched pair consists of one AA and one EA sample, matched for tumor grade and tumor subtype (based on immunohistochemical analysis of ER, PR, and HER2 status). 44 experiments; each experiment is tumor DNA versus reference control DNA (AF) isolated from the blood of a 25-year-old African-American female with no familial or personal history of breast cancer. Additional control experiments included the AF reference versus the well-characterized F1 reference, and 3 self-self hybridization controls (AF versus AF).
2013-01-29 | E-GEOD-26214 | biostudies-arrayexpress
Project description:In the United States, African-American (AA) women are more likely to develop early-onset breast cancer and have historically poorer outcomes due to this disease compared to European-American (EA) women. Here, we analyzed genomic profiles of breast tumors from young women (<50 years old), matched by tumor subtype, histological grade, and ethnicity (African-American, AA, compared to European-American, EA). DNA copy number alterations (CNAs) were analyzed on the Affymetrix Human SNP Array v 6.0 platform. The study provides insight into the genetic component of ethnicity-related breast cancer health disparities. DNA copy number alterations (CNAs) and genotypes were analyzed using the Affymetrix SNP 6.0 platform. Breast tumor samples from young women (< 50 years old) were matched as follows: a matched pair consists of one AA and one EA sample, matched for tumor grade and tumor subtype (based on immunohistochemical analysis of ER, PR, and HER2 status). DNA from forty-four samples (22 AA, 22 EA) was analyzed on the Affymetrix SNP 6.0 array according to manufacturer’s directions.
2013-01-29 | E-GEOD-26232 | biostudies-arrayexpress
Project description:Purpose: Black/African American (AA) women are twice as likely to be diagnosed with triple negative breast cancer (TNBC) compared to whites, an aggressive breast cancer subtype associated with poor prognosis. There are no routinely used targeted clinical therapies for TNBC; thus there is a clear need to identify prognostic markers and potential therapeutic targets. Methods: We evaluated expression of 27,016 genes in 155 treatment-naïve TN tumors from AA women in Detroit. Associations with survival were evaluated using Cox proportional hazards models adjusting for stage and age at diagnosis, and p-values were corrected using a false discovery rate. Our validation sample consisted of 158 TN tumors (54 AA) from The Cancer Genome Atlas (TCGA). Meta-analyses were performed to obtain summary estimates by combining TCGA and Detroit AA cohort results. Results: In the Detroit AA cohort, CLCA2 [Hazard ratio (HR)=1.56, 95% confidence interval (CI) 1.31-1.86, nominal p=5.1x10-7, FDR p=0.014], SPIC [HR=1.47, 95%CI 1.26-1.73, nominal p=1.8x10-6, FDR p=0.022], and MIR4311 [HR=1.57, 95% CI 1.31-1.92, nominal p=2.5x10-5, FDR p=0.022] expression were associated with overall survival. Further adjustment for treatment and breast cancer specific survival analysis did not substantially alter effect estimates. Meta-analysis with TCGA data showed that CLCA2 and SPIC were associated with overall survival for TNBC among AA women. Conclusions: We identified three potential prognostic markers for TNBC in AA women, for which SPIC may be an AA-specific prognostic marker.
2019-12-17 | GSE142102 | GEO
Project description:To investigate genetic and molecular differences that may exist between prostate cancers of African American and European American origin. Gene expression profile analysis was performed comparing RNA seq data of African American prostate cancer cell lines (inhouse) and European American prostate cancer cell lines (public repository)
2022-08-05 | GSE203338 | GEO
Project description:Newborn screening blood spots were obtained for neonates born to women enrolled in the Emory University African American Microbiome in Pregnacy Cohort
2021-07-01 | GSE154446 | GEO
Project description:We reAggressive high-grade, estrogen receptor negative (ER-) breast cancer is more common among American women of African ancestry (AA) than those of European ancestry (EA). The reasons remain largely unknown. Epigenetic mechanisms, particularly DNA methylation and altered microRNA (miRNA) expression, may contribute to racial differences in breast cancer. However, the characterization of this epigenetic modification in relation to ER+ and ER- breast cancer, and its functional role in the regulation of miRNA expression remains to be investigated, especially among high risk AA women. In this study, we evaluated methylation patterns of miRNA genes and their effect on miRNA expression in breast tumors from both AA and EA women. The genome-wide methylation screen identified a number of differentially methylated loci (DML) between ER- and ER+ tumor subtypes in tumors from both races, or specific to AA or EA women. Integrated analysis of DNA methylation and miRNA expression further identified certain DMLs whose methylation levels were significantly correlated with the expression of relevant miRNAs, such as multiple CpGs highly correlated with miR-190b and miR-135b. In summary, our results suggest that DNA methylation patterns in miRNA encoding genes differ between breast cancers according to cancer subtype and race, and that this altered methylation may affect miRNA expression. Further pathway analysis identified their potential role in modulating cancer-related key biological processes. These findings shed light on the epigenetic regulation of miRNA expression and provide insights into the relations of clinical-relevant miRNAs to their target genes and to serve as potential preventative and therapeutic targets. port the application of single-molecule-based sequencing technology for high-throughput profiling of histone modifications in mammalian cells. By obtaining over four billion bases of sequence from chromatin immunoprecipitated DNA, we generated genome-wide chromatin-state maps of mouse embryonic stem cells, neural progenitor cells and embryonic fibroblasts. We find that lysine 4 and lysine 27 trimethylation effectively discriminates genes that are expressed, poised for expression, or stably repressed, and therefore reflect cell state and lineage potential. Lysine 36 trimethylation marks primary coding and non-coding transcripts, facilitating gene annotation. Trimethylation of lysine 9 and lysine 20 is detected at satellite, telomeric and active long-terminal repeats, and can spread into proximal unique sequences. Lysine 4 and lysine 9 trimethylation marks imprinting control regions. Finally, we show that chromatin state can be read in an allele-specific manner by using single nucleotide polymorphisms. This study provides a framework for the application of comprehensive chromatin profiling towards characterization of diverse mammalian cell populations.
2021-01-01 | GSE156968 | GEO
Project description:We reAggressive high-grade, estrogen receptor negative (ER-) breast cancer is more common among American women of African ancestry (AA) than those of European ancestry (EA). The reasons remain largely unknown. Epigenetic mechanisms, particularly DNA methylation and altered microRNA (miRNA) expression, may contribute to racial differences in breast cancer. However, the characterization of this epigenetic modification in relation to ER+ and ER- breast cancer, and its functional role in the regulation of miRNA expression remains to be investigated, especially among high risk AA women. In this study, we evaluated methylation patterns of miRNA genes and their effect on miRNA expression in breast tumors from both AA and EA women. The genome-wide methylation screen identified a number of differentially methylated loci (DML) between ER- and ER+ tumor subtypes in tumors from both races, or specific to AA or EA women. Integrated analysis of DNA methylation and miRNA expression further identified certain DMLs whose methylation levels were significantly correlated with the expression of relevant miRNAs, such as multiple CpGs highly correlated with miR-190b and miR-135b. In summary, our results suggest that DNA methylation patterns in miRNA encoding genes differ between breast cancers according to cancer subtype and race, and that this altered methylation may affect miRNA expression. Further pathway analysis identified their potential role in modulating cancer-related key biological processes. These findings shed light on the epigenetic regulation of miRNA expression and provide insights into the relations of clinical-relevant miRNAs to their target genes and to serve as potential preventative and therapeutic targets. port the application of single-molecule-based sequencing technology for high-throughput profiling of histone modifications in mammalian cells. By obtaining over four billion bases of sequence from chromatin immunoprecipitated DNA, we generated genome-wide chromatin-state maps of mouse embryonic stem cells, neural progenitor cells and embryonic fibroblasts. We find that lysine 4 and lysine 27 trimethylation effectively discriminates genes that are expressed, poised for expression, or stably repressed, and therefore reflect cell state and lineage potential. Lysine 36 trimethylation marks primary coding and non-coding transcripts, facilitating gene annotation. Trimethylation of lysine 9 and lysine 20 is detected at satellite, telomeric and active long-terminal repeats, and can spread into proximal unique sequences. Lysine 4 and lysine 9 trimethylation marks imprinting control regions. Finally, we show that chromatin state can be read in an allele-specific manner by using single nucleotide polymorphisms. This study provides a framework for the application of comprehensive chromatin profiling towards characterization of diverse mammalian cell populations.
2021-01-01 | GSE156969 | GEO
Project description:The incidence and mortality rates of prostate cancer are significantly higher in African-American men when compared to European-American men. We tested the hypothesis that differences in tumor biology contribute to this survival health disparity. Using microarray technology, we obtained gene expression profiles of primary prostate tumors resected from 33 African-American and 36 European-American patients. These tumors were matched on clinical parameters. We also evaluated 18 non-tumor prostate tissues from 7 African-American and 11 European-American patients. The resulting datasets were analyzed for expression differences on the gene and pathway level comparing African-American with European-American patients. Our analysis revealed a significant number of genes, e.g., 162 transcripts at a false-discovery rate less than 5%, to be differently expressed between African-American and European-American patients. Using a disease association analysis, we identified a common relationship of these transcripts with autoimmunity and inflammation. These findings were corroborated on the pathway level with numerous differently expressed genes clustering in immune response, stress response, cytokine signaling, and chemotaxis pathways. Furthermore, a two-gene tumor signature was identified that accurately differentiated between African-American and European-American patients. This finding was confirmed in a blinded analysis of a second sample set. In conclusion, the gene expression profiles of prostate tumors indicate prominent differences in tumor immunobiology between African-American and European-American men. The profiles portray the existence of a distinct tumor microenvironment in these two patient groups. Keywords: Microdissected tissue analysis
2008-01-01 | GSE6956 | GEO