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Oncopig and Human Bladder Cancer Cell Lines: Control vs Gemcitabine Treated

ABSTRACT: Oncopig and Human Bladder Cancer Cell Lines: Control vs Gemcitabine Treated

PROVIDER: PRJNA1073916 | ENA |

REPOSITORIES: ENA

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Oncopig and Human Bladder Cancer Cell Lines: Control vs Gemcitabine Treated

Project description:Transcriptional profiling of Oncopig and human bladder cancer cell lines comparing control untreated cells to cell treated with gemcitabine for 48 hours. Goal was to compare similar transcriptional alterations in response to gemcitabine treatment across both species

2024-02-16 | GSE255187 | GEO

Gene Expression of human bladder cancer cell line RT112 and Gemcitabine Resistant Bladder Cancer cell line RT112-Gr

Project description:In this research, Human OneArray Microarray analysis was performed to obtain broad spectrum information about the genes differentially expressed in human bladder cancer cell line RT112 and Gemcitabine Resistant Bladder Cancer cell line RT112-Gr.

2015-04-16 | E-MTAB-3495 | biostudies-arrayexpress

Enzalutamide inhibits proliferation of gemcitabine-resistant bladder cancer cells with increased androgen receptor expression

Project description:Advanced bladder cancer is treated mainly with gemcitabine and cisplatin, but most patients eventually become resistance to these chemotherapeutic agents. Androgen receptor (AR) signaling has been implicated in bladder cancer as well as other types of cancer including prostate cancer. In the present study, we showed the expression and role of AR in gemcitabine-resistant bladder cancer cells and examined the potential of enzalutamide, an AR inhibitor, as a therapeutic for the chemoresistance. First of all, we established gemcitabine-resistant T24 cells (T24GR) from T24 bladder cancer cells and performed gene expression profiling and network analysis, which revealed increased AR expression and AR-related gene network in T24GR cells. Quantitative RT-PCR and Western blot analysis confirmed increased expression of AR in T24GR cells compared with parental T24 cells, which was associated with more potent transcriptional activity of AR in T24GR cells. The number of AR gene copy in T24GR cells was twice as many as that of T24 cells. Knockdown of AR expression by siRNA resulted in inhibition of proliferation of T24GR cells. Cell culture in charcoal-stripped serum and treatment with enzalutamide also inhibited growth of T24GR cells, which was accompanied by cell cycle arrest. Lastly, the AR transcriptional activity was found to be reduced in T24GR cells by enzalutamide treatment. Our results suggest that blockade of AR signaling by enzalutamide might be effective for patients with advanced gemcitabine-resistant bladder cancer with increased AR expression.

2016-11-30 | GSE77883 | GEO

Urinary bladder in F344 rats: Control vs dimethylarsinic acid

Project description:Urinary bladder in F344 rats: Control vs dimethylarsinic acid

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Project description:Pancreatic cancer cells (MIA PaCa-2) were treated with Gemcitabine and overall protein changes were studied

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Project description:Gemcitabine (GEM) is a key drug for treating PDAC, and it is commonly used for adjuvant chemotherapy. Although the majority of PDAC is sensitive to GEM at first, GEM cannot control PDAC for very long, suggesting that PDAC develops resistance to GEM after prolonged exposure. No reliable predictors of susceptibility to gemcitabine chemotherapy exist in pancreatic ductal adenocarcinoma. This study assesses gemcitabine resistant PDAC for its specific mRNA expression pattern. Gemcitabine resistant variants of Panc1, a human pancreatic adenocarcinoma cell line, were established. mRNA screening was investigated by microarray.

2016-04-26 | GSE80617 | GEO

microRNA Expression profiles of parental Panc1 cell lines and Gemcitabine resistance Panc1 cell lines

Project description:Gemcitabine (GEM) is a key drug for treating PDAC, and it is commonly used for adjuvant chemotherapy. Although the majority of PDAC is sensitive to GEM at first, GEM cannot control PDAC for very long, suggesting that PDAC develops resistance to GEM after prolonged exposure. No reliable predictors of susceptibility to gemcitabine chemotherapy exist in pancreatic ductal adenocarcinoma. MicroRNAs (miR) are epigenetic gene regulators with tumorsuppressive or oncogenic roles in various carcinomas. This study assesses gemcitabine resistant PDAC for its specific miR expression pattern. Gemcitabine resistant variants of Panc1, a human pancreatic adenocarcinoma cell line, were established. MicroRNA screening was investigated by microarray.

2016-04-26 | GSE80616 | GEO

Urinary bladder in F344 rats: Control vs dimethylarsinic acid-induced tumors

Project description:Urinary bladder in F344 rats: Control vs dimethylarsinic acid-induced tumors

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Expression data from gemcitabine treated pancreatic CAFs

Project description:Pancreatic ductal adenocarcinoma (PDAC) has a characteristically dense stroma comprised predominantly of cancer associated fibroblasts (CAFs). CAFs promote tumor growth, metastasis and treatment resistance. We aimed to investigate the molecular changes and functional consequences associated with chemotherapy treatment of PDAC CAFs. Chemoresistant immortalized CAFs (R-CAFs) were generated by continuous incubation in 100nM gemcitabine. Gene expression differences between treatment naÃ¯ve CAFs (N-CAFs) and R-CAFs were compared by array analysis. Immortalized human pancreatic CAFs were grown for 30 days in either control media or media containing 100nM gemcitabine. RNA was then isolated and hybidized on U133 Plus 2.0 Affymetrix arrays.

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