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RNA data of NCI-H446 tumours treated with ERY974 and/or paclitaxel in huNOG mice.

ABSTRACT: We found that ERY974 shows only moderate antitumor efficacy in NCI-H446 non-inflamed tumor in huNOG mice. We also observed that ERY974 + paclitaxel increases antitumour efficacy in non-inflamed NCI-H446 tumours. To identify a mechanism of combination effect, we compared RNA expression of NCI-H446 tumors treated with ERY974, cisplatin, or combination.

ORGANISM(S): Mus musculus Homo sapiens

PROVIDER: GSE211374 | GEO | 2022/08/21

REPOSITORIES: GEO

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RNA data of NCI-H446 tumours treated with ERY974 and/or cisplatin in huNOG mice

Project description:We found that ERY974 shows only moderate antitumor efficacy in NCI-H446 non-inflamed tumor in huNOG mice. We also observed that ERY974 + cisplatin increases antitumour efficacy in non-inflamed NCI-H446 tumours. To identify a mechanism of combination effect, we compared RNA expression of NCI-H446 tumors treated with ERY974, cisplatin, or combination.

2022-08-22 | GSE211514 | GEO

NCI-H446 control (NC) and MTA1-overexpressing (OE) cells

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RNA data of MKN45 tumours treated with ERY974 and/or capecitabine in huNOG mice

Project description:We found that ERY974 shows only moderate antitumor efficacy in MKN45 non-inflamed tumor in huNOG mice. We also observed that ERY974 + capecitabine increases antitumour efficacy in non-inflamed MKN45 tumours. To identify a mechanism of combination effect, we compared RNA expression of MKN45 tumors treated with ERY974, capecitabine, or combination.

2022-08-21 | GSE211373 | GEO

Paclitaxel resistance in ovarian cancer increases oncolytic adenovirus efficacy via upregulated CAR expression and dysfunctional cell cycle control

Project description:The microtubule-stabilising drug paclitaxel has activity in relapsed ovarian cancer. However, resistance frequently develops. Oncolytic adenoviruses are a novel cancer therapy, and replicate selectively within and lyse malignant cells, leading to productive infection of neighbouring cells. We found increased efficacy of adenoviruses of multiple subtypes in paclitaxel-resistant ovarian cancer cells. There was increased expression of a key adenovirus receptor, CAR (coxsackie adenovirus receptor), due to increased transcription that resulted from histone modification. Moreover, CAR transcription increased in intraperitoneal xenografts with acquired paclitaxel resistance and in tumours from patients with paclitaxel-resistant ovarian cancer. Finally, we identified dysregulated cell cycle control as a second mechanism of increased adenovirus efficacy in paclitaxel-resistant ovarian cancer and that inhibition of CDK4/6 using PD-0332991 was able both to reverse paclitaxel resistance and reduce adenovirus efficacy. Thus, paclitaxel resistance increases oncolytic adenovirus efficacy via at least two separate mechanisms. Parental SKOV3 and paclitaxel-resistant SKOV3-TR cells were analysed in duplicate

2015-12-10 | E-GEOD-54772 | biostudies-arrayexpress

Paclitaxel resistance in ovarian cancer increases oncolytic adenovirus efficacy via upregulated CAR expression and dysfunctional cell cycle control

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Comparison of genome-wide DNA methylation between H446/DDP and H446

Project description:Little has been known about the genome-wide methylation frameworks of the chemo-resistant cells of SCLC currently, which might provide prospective layouts to discover the genes and the signal pathways related with chemo-resistance of SCLC. Thus, this research reported for the first time the genome-wide abnormal methylation pattern of chemo-resistant H446/DDP cells of human SCLC induced by the cisplatin

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Paclitaxel resistant MDA-MB-231 Cells and resensitization with bexarotene treatment

Project description:Acquired drug resistance represents a major challenge in chemo-therapy treatment for various types of cancers. We have found that the retinoid X receptorâselective agonist bexarotene (LGD1069, Targretin) was efficacious in treating chemo-resistant cancer cells. The goal of this microarray study was to understand the mechanism of bexaroteneâs role in overcoming acquired drug resistance using human breast cancer cells MDA-MB-231 as a model system and paclitaxel as model compound. After MDA-MB-231 cells were repeatedly treated with paclitaxel for 8 cycles with each cycle including a 3-day treatment with 30 nM paclitaxel and followed by a 7-day exposure to control medium, MDA cells resistant to paclitaxel were developed and their growth was no longer inhibited by paclitaxel treatment. Those MDA cells with acquired drug resistance, when treated with paclitaxel and bexarotene in combination, could regain their sensitivity and their growth were again inhibited. Therefore, RNA samples from parental MDA-MB-231 cells, paclitaxel-resistant MDA cells treated with vehicle, paclitaxel alone or in combination with bexarotene, were used for perform global gene expression profiling with Affymetrix HG-U133A gene chips. Keywords: Drug Treatment MDA-MB-231 cells were exposed to regimens on a 10-day cycle: a 3-day treatment with 30 nM paclitaxel and followed by a 7-day exposure to control medium. Paclitaxel resistant MDA-MB-231 cells (MDA-PR) were established within 8 cycles of such treatment (80 days). These MDA-PR cells were then treated with vehicle control, paclitaxel along, or the combination of 30 nM paclitaxel ( 3 days on and 7 days off) and 1 ÂµM Targretin (10 days on) in a new 10-day cycle for 3 months. Thus, there are four treatment groups, parent MDA cells, MDA-PR, MDA-PR treated with paclitaxel, MDA-PR treated with paclitaxel and bexarotene, and each group had four biological replicates.

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Paclitaxel resistant MDA-MB-231 Cells and resensitization with bexarotene treatment

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Gene expression difference of small cell lung cancer cell after treatment with a kind of drug.

Project description:Examine gene expression changes of NCI-H446 after treatment with a kind of chemotheraputic drug

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2023-07-07 | GSE236502 | GEO

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