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GSE5847
Homo sapiens
95 Downloadable Samples
Affymetrix Human Genome U133A Array (hgu133a)
Description
Tumor epithelium and surrounding stromal cells were isolated using laser capture microdissection of human breast cancer to examine differences in gene expression based on tissue types from inflammatory and non-inflammatory breast cancer
Publication Title
A stromal gene signature associated with inflammatory breast cancer.
Sample Metadata Fields
Specimen part, Disease, Race, Subject
View Samples- Homo sapiens
- 79 Downloadable Samples
- Affymetrix Human Genome U133A 2.0 Array (hgu133a2)
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.
Publication Title
Tumor immunobiological differences in prostate cancer between African-American and European-American men.
Sample Metadata Fields
Race
View Samples- Homo sapiens
- 47 Downloadable Samples
- Affymetrix Human Genome U133A 2.0 Array (hgu133a2)
Description
BACKGROUND. Perineural invasion (PNI) is the dominant pathway for local invasion in prostate cancer. To date, only few studies have investigated the molecular differences between prostate tumors with PNI and those without it.
Publication Title
Expression of microRNAs and protein-coding genes associated with perineural invasion in prostate cancer.
Sample Metadata Fields
Race
View Samples- Homo sapiens
- 50 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
In order to identify biologically relevant tumor markers, and novel therapeutic target we have compared the tumor gene expression profiles of long (OS>=24 months,n=14) and short (OS <=7months, n=11) survival patients. Then we conducted Kaplan-Meier survival analysis using all the 50 samples listed here. The Affymetrix gene-expression data of these 50 samples were also included in the earlier submission by us as GEO accession number GSE62452.
Publication Title
Endothelial Nitric Oxide Synthase Traffic Inducer (NOSTRIN) is a Negative Regulator of Disease Aggressiveness in Pancreatic Cancer.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 15 Downloadable Samples
- Affymetrix Human Genome U133A 2.0 Array (hgu133a2)
Description
MicroRNAs (miRs) are small non-coding RNAs that can function as tumor suppressor genes. We previously reported that miR-1 is among the most consistently down-regulated miRs in primary human prostate tumors. In this follow-up study, we further corroborated this finding in an independent dataset and made the novel observation that miR-1 expression is further reduced in distant metastasis and is a predictor of disease recurrence. Moreover, we performed in vitro experiments to explore the candidate tumor suppressor function of miR-1. Cell-based assays showed that miR-1 is epigenetically silenced in human prostate cancer cells. Overexpression of miR-1 in these cells led to growth inhibition and down-regulation of genes in pathways regulating cell cycle progression, mitosis, DNA replication/repair, and actin dynamics. This observation was further corroborated with protein expression analysis and 3-UTR-based reporter assays, indicating that genes in these pathways are either direct or indirect targets of miR-1. A gene set enrichment analysis revealed that miR-1-mediated tumor suppressor effects are globally similar to those of histone deacetylase inhibitors. Lastly, we obtained preliminary evidence that miR-1 alters gH2A.X marker expression and affects the cellular organization of F-actin and filipodia formation. In conclusion, our findings indicate that miR-1 acts as a tumor suppressor in prostate cancer by influencing multiple cancer-related processes and by inhibiting cell proliferation and motility.
Publication Title
MicroRNA-1 is a candidate tumor suppressor and prognostic marker in human prostate cancer.
Sample Metadata Fields
Cell line, Treatment
View Samples- Homo sapiens
- 90 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
In order to identify biologically relevant tumor markers with prognostic significance, we set out to analyze gene expression profiling of tumor and adjacent non-tumor tissues from PDAC cases.
Publication Title
DPEP1 inhibits tumor cell invasiveness, enhances chemosensitivity and predicts clinical outcome in pancreatic ductal adenocarcinoma.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus, Homo sapiens
- 52 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st), Affymetrix Human Genome U133A 2.0 Array (hgu133a2)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
An Immune-Inflammation Gene Expression Signature in Prostate Tumors of Smokers.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Homo sapiens
- 30 Downloadable Samples
Affymetrix Human Genome U133A 2.0 Array (hgu133a2)
Description
Current smokers develop metastatic prostate cancer more frequently than nonsmokers, suggesting that a tobacco-derived factor induces metastasis. To identify smoking-induced alterations in human prostate tumors, we analyzed gene and protein expression of tumors from current, past, and never smokers and observed distinct molecular alterations in current smokers. Specifically, an immune and inflammation signature was identified in prostate tumors of current smokers that was either attenuated or absent in past and never smokers. Key characteristics of this signature included augmented immunoglobulin expression by tumor-infiltrating B cells, NF-kB activation, and increased interleukin-8 in tumor and blood. In an alternate approach to characterize smoking-induced oncogenic alterations, we explored the effects of nicotine in prostate cancer cells and prostate cancer-prone TRAMP mice. These experiments showed that nicotine increases both invasiveness of human prostate cancer cells and metastasis in tumor-bearing TRAMP mice, indicating that nicotine can induce a phenotype that resembles the epidemiology of smoking-associated prostate cancer progression. In summary, we describe distinct oncogenic alterations in prostate tumors from current smokers and show that nicotine can enhance prostate cancer metastasis.
Publication Title
An Immune-Inflammation Gene Expression Signature in Prostate Tumors of Smokers.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 12 Downloadable Samples
- Affymetrix Human Genome U133A 2.0 Array (hgu133a2)
Description
Current smokers develop metastatic prostate cancer more frequently than nonsmokers, suggesting that a tobacco-derived factor induces metastasis. To identify smoking-induced alterations in human prostate tumors, we analyzed gene and protein expression of tumors from current, past, and never smokers and observed distinct molecular alterations in current smokers. Specifically, an immune and inflammation signature was identified in prostate tumors of current smokers that was either attenuated or absent in past and never smokers. Key characteristics of this signature included augmented immunoglobulin expression by tumor-infiltrating B cells, NF-kB activation, and increased interleukin-8 in tumor and blood. In an alternate approach to characterize smoking-induced oncogenic alterations, we explored the effects of nicotine in prostate cancer cells and prostate cancer-prone TRAMP mice. These experiments showed that nicotine increases both invasiveness of human prostate cancer cells and metastasis in tumor-bearing TRAMP mice, indicating that nicotine can induce a phenotype that resembles the epidemiology of smoking-associated prostate cancer progression. In summary, we describe distinct oncogenic alterations in prostate tumors from current smokers and show that nicotine can enhance prostate cancer metastasis.
Publication Title
An Immune-Inflammation Gene Expression Signature in Prostate Tumors of Smokers.
Sample Metadata Fields
Cell line
View Samples- Mus musculus
- 10 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
Current smokers develop metastatic prostate cancer more frequently than nonsmokers, suggesting that a tobacco-derived factor induces metastasis. To identify smoking-induced alterations in human prostate tumors, we analyzed gene and protein expression of tumors from current, past, and never smokers and observed distinct molecular alterations in current smokers. Specifically, an immune and inflammation signature was identified in prostate tumors of current smokers that was either attenuated or absent in past and never smokers. Key characteristics of this signature included augmented immunoglobulin expression by tumor-infiltrating B cells, NF-kB activation, and increased interleukin-8 in tumor and blood. In an alternate approach to characterize smoking-induced oncogenic alterations, we explored the effects of nicotine in prostate cancer cells and prostate cancer-prone TRAMP mice. These experiments showed that nicotine increases both invasiveness of human prostate cancer cells and metastasis in tumor-bearing TRAMP mice, indicating that nicotine can induce a phenotype that resembles the epidemiology of smoking-associated prostate cancer progression. In summary, we describe distinct oncogenic alterations in prostate tumors from current smokers and show that nicotine can enhance prostate cancer metastasis.
Publication Title
An Immune-Inflammation Gene Expression Signature in Prostate Tumors of Smokers.
Sample Metadata Fields
Specimen part
View Samples