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Identify genes modulated by gemcitabine and/or GNE-783 in HT-29 tumors in vivo

ABSTRACT: Identified genes that were up- or down-regulated in HT-29 xenograft tissue in response to the indicated treatments.

ORGANISM(S): Homo sapiens

PROVIDER: GSE61802 | GEO | 2017/09/01

SECONDARY ACCESSION(S): PRJNA262164

REPOSITORIES: GEO

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Identify genes modulated by gemcitabine and/or GNE-783

Project description:Identified genes that were up- or down-regulated in HT-29 cells in response to the indicated treatments.

2017-09-01 | GSE61795 | GEO

Modulated electro-hyperthermia related mRNA expression profile development in HT-29 xenograft mouse model.

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Bevacizumab-resistant HT-29 tumors vs untreated control

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Modulated electro-hyperthermia related mRNA expression profile development in HT-29 xenograft mouse model.

Project description:HT-29 human colorectal adenocarcinoma cells were xenografted into both femoral regions of 6 to 8-week old Balb/c (nu/nu) mice. After 18 days electromagnetic heat treatment was performed. We used microarray technology to identify the heat treatment releted gene expression alterations using human tumor xenograft mouse model. Fresh frozen tissue sections were performed from the xenograft and tumorous regions were microdissected for total RNA isolation and gene expression analysis purposes.

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Peripheral regions and central regions from HT-29 tumors

Project description:Gene expression of peripheral regions and central regions from HT-29 tumors

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Identify genes modulated by a 5 uM 30-minute pulse dose of gemcitabine

Project description:Identified genes that were up- or down-regulated in HT-29 cells in response to gemcitabine

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Expression data of colorectal cancer HT-29 cells

Project description:Colorectal cancer HT-29 cell line is a comonly-used human cancer cell line. We have used this cell line for examining the effect of various anticancer compounds on gene expression and we obtained gene expression data of untreated HT-29 cells as a control data for the analysis.

2017-06-14 | GSE99968 | GEO

HT-29 cells treated with IFN-γ

Project description:Expression data from HT-29 human colon adenocarcinoma cells treated with IFN-γ for 24 hr

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Integration of genomic and proteomic data to identify candidate genes in HT-29 cells after incubation with Bifidobacterium bifidum ATCC 29521

Project description:Identify candidate different expression genes in HT-29 cells after incubation with Bifidobacterium bifidum ATCC 29521. The results of microarray provide importment information for different genes expression in HT-29 cell after incubation withBifidobacterium bifidum ATCC 29521, up or down-regulated.

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Folic Acid study in HT-29 cells

Project description:Low intracellular folate levels diminish the growth rate of HT-29 human colon cancer cells. This is accompanied by a metabolic shift from cytosolic glycolysis towards mitochondrial oxidative phosphorylation, as demonstrated by a lower lactate production and an increased mitochondrial oxygen consumption rate. To obtain insight in the molecular effects underlying these changes, the steady state gene expression profiles of HT-29 cells with different intracellular folate concentrations were compared. The gene expression profile of HT-29 cells with low intracellular folate levels (grown for 3 weeks in 10 ng/ml folic acid (PGA)) was clearly distinct from that of the other exposure conditions, which provide sufficient intracellular folate levels (100 ng/ml PGA, 10 ng/ml methyltetrahydrofolate (MTHF) or 100 ng/ml MTHF). Intracellular folate deficiency, contrary to expectation, did not lead to major changes in expression of genes involved in energy metabolism. This suggests that the shift towards mitochondrial oxidative phosphorylation is not mediated at the transcription level. Furthermore, only minor changes in the expression of folate metabolism related genes were observed. The changes that were observed were consistent with nucleotide salvage and in agreement with nucleotide need of the slow-growing folate-deficient HT-29 cells. The major observed effects were on cell cycle related gene expression, which was increased and interferon-responsive gene expression, which was reduced. The increase in cell cycle related gene expression seems compensatory to the reduced cell growth. Down-regulation of the interferon-response may be explained by decreased expression of signal transducer and activator of transcription 1 upon folate deficiency. Keywords: dose response, folic acid, HT-29 cells, human

2005-08-13 | GSE3099 | GEO

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