Prostate_5azadC
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE2932 | GEO | 2006/05/08
SECONDARY ACCESSION(S): PRJNA92437
REPOSITORIES: GEO
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Project description:This microarray dataset accompanies the publication by Kim et al, "The retinoic acid synthesis gene ALDH1a2 is a candidate tumor suppressor in prostate cancer". The dataset comprises four prostate cancer cell lines treated with the DNA methyltransferase inhibitor 5-aza-dC. For each cell line, gene expression in treated (channel 2; Cy5) and untreated (channel 1; Cy3) cells is directly compared by hybridization to the same DNA microarray. Further details on the treatment conditions are provided in the manuscript. A compound treatment design type is where the response to administration of a compound or chemical (including biological compounds such as hormones) is assayed. Keywords: compound_treatment_design
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Project description:This microarray dataset accompanies the publication by Kim et al, "The retinoic acid synthesis gene ALDH1a2 is a candidate tumor suppressor in prostate cancer". The dataset comprises four prostate cancer cell lines treated with the DNA methyltransferase inhibitor 5-aza-dC. For each cell line, gene expression in treated (channel 2; Cy5) and untreated (channel 1; Cy3) cells is directly compared by hybridization to the same DNA microarray. Further details on the treatment conditions are provided in the manuscript. A compound treatment design type is where the response to administration of a compound or chemical (including biological compounds such as hormones) is assayed. Using regression correlation
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Project description:This microarray dataset accompanies the publication by Kim et al, "The retinoic acid synthesis gene ALDH1a2 is a candidate tumor suppressor in prostate cancer". The dataset comprises four prostate cancer cell lines treated with the DNA methyltransferase inhibitor 5-aza-dC. For each cell line, gene expression in treated (channel 2; Cy5) and untreated (channel 1; Cy3) cells is directly compared by hybridization to the same DNA microarray. Further details on the treatment conditions are provided in the manuscript.
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Project description:This set of arrays contains 31 experiments. It is designed to determine the effects of methylseleninic acid on the transcriptional program of prostate cancer LNCaP cells. Threee concentrations, 3, 10, and 30 uM, were used for treatment. The effects were monitored through a time course of 48 hours, with samples collected at 10 different time points (1, 2, 4, 6, 9, 12, 15, 18, 24, and 48). RNA from treated cells were labeled using Cy5, and untreated using Cy3. One experiment using RNA from untreated cells in both channel was used as control. A compound treatment design type is where the response to administration of a compound or chemical (including biological compounds such as hormones) is assayed. Keywords: compound_treatment_design
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Project description:BACKGROUND. Prostate cancer is thought to arise as a result of oxidative stresses and induction of antioxidant electrophile defense (phase 2) enzymes has been proposed as a prostate cancer prevention strategy. The isothiocyanate sulforaphane, derived from cruciferous vegetables like broccoli, potently induces surrogate markers of phase 2 enzyme activity in prostate cells in vitro and in vivo. To better understand the temporal effects of sulforaphane and broccoli sprouts on gene expression in prostate cells, we carried out comprehensive transcriptome analysis using cDNA microarrays. METHODS. Transcripts significantly modulated by sulforaphane over time were identified using StepMiner analysis. Ingenuity Pathway Analysis (IPA) was used to identify biological pathways, networks, and functions significantly altered by sulforaphane treatment. . StepMiner and IPA revealed significant changes in many transcripts associated with cell growth and cell cycle, as well as a significant number associated with cellular response to oxidative damage and stress. Comparison to an existing dataset suggested that sulforaphane blocked cell growth by inducing G2/M arrest. Cell growth assays and flow cytometry analysis confirmed that sulforaphane inhibited cell growth and induced cell cycle arrest. CONCLUSIONS. Our data suggest that in prostate cells sulforaphane primarily induces cellular defenses and inhibits cell growth by causingG2/Mphase arrest. Furthermore, based on the striking similarities in the gene expression patterns induced across experiments in these cells, sulforaphane appears to be the primary bioactive compound present in broccoli sprouts, suggesting that broccoli sprouts can serve as a suitable source for sulforaphane in intervention trials. A compound treatment design type is where the response to administration of a compound or chemical (including biological compounds such as hormones) is assayed. Time: length of treatment Compound Based Treatment: LNCaP cells were treated with 10 or 25 uM L-sulforaphane, broccoli extract or DMSO Keywords: compound_treatment_design
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2008-04-01 | E-GEOD-10655 | biostudies-arrayexpress
Project description:The dataset comprises array CGH data of 64 prostate cancer specimens performed on Stanford cDNA microarrays, to accompany the study of J Lapointe et al (2007). For each array, Channel 2 represents Cy5-labeled prostate genomic DNA, and Channel 1 Cy3-labeled normal male genomic DNA. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Using regression correlation
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