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Gene Expression analysis comparison between control and CC214-2 resistant GBM39 xenografts

ABSTRACT: Here we present gene expression analysis data on two vehicle treated and two CC214-2 (an mTOR kinase inhibitor) resistant GlioBlastoma Multiforme 39 (GBM39) xenografts, showing that the expressioin profiles of 88 genes are significantly different between the two groups.

ORGANISM(S): Homo sapiens

PROVIDER: GSE63387 | GEO | 2014/11/19

SECONDARY ACCESSION(S): PRJNA267641

REPOSITORIES: GEO

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Gene Expression analysis comparison between control and CC214-2 resistant GBM39 xenografts

Project description:Here we present gene expression analysis data on two vehicle treated and two CC214-2 (an mTOR kinase inhibitor) resistant GlioBlastoma Multiforme 39 (GBM39) xenografts, showing that the expressioin profiles of 88 genes are significantly different between the two groups. GBM39 primary neurospheres were cultured in standard cancer stem cell medium conditions and then were injected in the mice flanks to generate xenograft tissues. Mice carrying CC214-2 resistant xenografts were treated with a solution of CC214-2 once every two days, by gavage, for 40 days. Total RNA was extracted from GBM39 control and CC214-2 resistant xenografts using the Qiagen RNA micro kit protocol and analysed by Affymetrix U133 plus 2.0 array

2014-11-19 | E-GEOD-63387 | biostudies-arrayexpress

Copy number variation comparison between control and CC214-2 resistant GBM39 xenografts

Project description:Here we present genome-wide copy number variation data on two vehicle treated and two CC214-2 (an mTOR kinase inhibitor) resistant GlioBlastoma Multiforme 39 (GBM39) xenografts, showing the absence of significant differences between the two groups, demonstrating that resistance to CC214-2 is due to adaptation rather than gene mutations.

2013-12-06 | GSE53042 | GEO

Copy number variation comparison between control and CC214-2 resistant GBM39 xenografts

2013-12-06 | E-GEOD-53042 | biostudies-arrayexpress

Glioblastoma Orthotopic Xenograft Transcriptome

Project description:Transcriptional profiling of glioblastoma orthotopic xenografts Descriptive experiment, comparison of 39 glioblastoma tumors as orthotopic xenografts

2012-07-10 | E-GEOD-38814 | biostudies-arrayexpress

Glioblastoma Xenograft Comparative Genomic Hybridization Arrays

Project description:DNA copy number profiling of 32 glioblastoma orthotopic xenografts Descriptive experiment, comparison of 39 glioblastoma tumors as orthotopic xenografts flow sorted for anueploidy

2012-07-10 | E-GEOD-38815 | biostudies-arrayexpress

Jung2019 - Regulating glioblastoma signaling pathways and anti-invasion therapy - core control model

Project description:This model is based on paper: Strategies in regulating glioblastoma signaling pathways and anti-invasion therapy Abstract: Glioblastoma multiforme is one of the most invasive type of glial tumors, which rapidly grows and commonly spreads into nearby brain tissue. It is a devastating brain cancer that often results in death within approximately 12 to 15 months after diagnosis. In this work, optimal control theory was applied to regulate intracellular signaling pathways of miR-451–AMPK–mTOR–cell cycle dynamics via glucose and drug intravenous administration infusions. Glucose level is controlled to activate miR-451 in the up-stream pathway of the model. A potential drug blocking the inhibitory pathway of mTOR by AMPK complex is incorporated to explore regulation of the down-stream pathway to the cell cycle. Both miR-451 and mTOR levels are up-regulated inducing cell proliferation and reducing invasion in the neighboring tissues. Concomitant and alternating glucose and drug infusions are explored under various circumstances to predict best clinical outcomes with least administration costs.

2020-03-03 | BIOMD0000000828 | BioModels

Jung2019 - egulating glioblastoma signaling pathways and anti-invasion therapy cell cycle dynamics model

Project description:This model is based on paper, based on its cell cycle dynamics model: Strategies in regulating glioblastoma signaling pathways and anti-invasion therapy Abstract: Glioblastoma multiforme is one of the most invasive type of glial tumors, which rapidly grows and commonly spreads into nearby brain tissue. It is a devastating brain cancer that often results in death within approximately 12 to 15 months after diagnosis. In this work, optimal control theory was applied to regulate intracellular signaling pathways of miR-451–AMPK–mTOR–cell cycle dynamics via glucose and drug intravenous administration infusions. Glucose level is controlled to activate miR-451 in the up-stream pathway of the model. A potential drug blocking the inhibitory pathway of mTOR by AMPK complex is incorporated to explore regulation of the down-stream pathway to the cell cycle. Both miR-451 and mTOR levels are up-regulated inducing cell proliferation and reducing invasion in the neighboring tissues. Concomitant and alternating glucose and drug infusions are explored under various circumstances to predict best clinical outcomes with least administration costs.

2019-10-02 | BIOMD0000000829 | BioModels

RNA seq NVP-BEZ235 treatment of U87MG cells

Project description:Glioblastoma (GBM) is the most lethal primary brain cancer that lacks effective molecular targeted therapies. PI3K/AKT/mTOR signaling pathway is activated in 90% of all Glioblastoma Multiforme (GBM) tumors. To gain insight into the impact of the PI3K Pathway on GBM metabolism, we treated U87MG GBM cells with 50nM NVP-BEZ235 (PI3K and mTOR a dual inhibitor) for four days and identified differentially expressed genes with RNA-seq analysis.

2021-12-01 | GSE179667 | GEO

The effect of GPR30 agonist G-1 on androgen-sensitive and castration-resistant LNCaP xenografts

Project description:G-1 is an agonist to GPR30. Activation of GPR30 by G-1 inhibited prostate cancer cell growth in LNCaP xenografts regrown after catration of the host (nude mice), but not in the androgen-sensitive LNCaP xenograft grown in an intact host. Results provide insights into the molecular basis of G-1 action in castration-resistant prostate cancer. Male nude mice were injected with LNCaP cells. When the LNCaP tumors reached 150–300 mm3, mice were divided into two groups: intact (androgen-sensitive tumor) and castrated. For the intact group, mice were subcutaneously injected with vehicle alone (95% PBS, 2.5% DMSO, 2.5% ethanol) or G-1 (4 mg/kg/day in vehicle) daily for 16 days. For the castrated group, tumors regressed and then regrew to ~300-400mm3. Mice were treated daily with vehicle or G-1 as described for 16 days. Tumors were harvested for RNA extraction and microarray experiments.

2014-02-14 | E-GEOD-54974 | biostudies-arrayexpress

Comprehensive genomic profiling of matched glioblastoma tumors, cell-lines and xenografts reveals genomic stability and adaptation to disparate growth environments

Project description:Glioblastoma Multiforme (GBM) is the most deadly brain tumor, and currently lacks effective treatment options. Brain tumor initiating cells (BTICs) and orthotopic xenografts are widely used in investigating GBM biology and new therapies for this aggressive disease. However, the genomic characteristics and molecular resemblance of these models to GBM tumors remain undetermined. We used massively parallel sequencing technology to decode the genomes and transcriptomes of BTICs and xenografts and their matched tumors in order to delineate the potential impacts of the distinct growth environments. Using data generated from whole‐genome sequencing of 201 samples and RNA sequencing of 118 samples, we showed that typical GBM genomic driver alterations found in the tumors were retained in BTICs and xenografts. In contrast, gene expression and methylation profiles indicated higher levels of divergence, likely due to the different growth environment for each sample type. These findings suggest that a comprehensive genomic understanding of in vitro and in vivo GBM model systems is crucial for interpreting data from drug‐screens, and can help control for biases introduced by cell culture conditions and the microenvironment in mouse models.

2019-03-22 | GSE128654 | GEO

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