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Regulation of gene expressions in vivo by anti-VEGF and anti-Notch therapy [Mouse430_2]

ABSTRACT: U87-EV human glioblastoma xenograft tumours is therapeutically treated by bevacizumab, a humanized anti-human VEGF mAb, or dibenzazepine (DBZ) when tumour is established in BALB/c SCID mice. At the end point, collect tumour samples and extracted total RNA for microarray to investigate the gene profile changes compared to control. These include the genes from human tumour cells and mouse host stroma cells. 5 control, 5 dibenzazepine-treated, and 4 bevacizumab-treated samples

ORGANISM(S): Mus musculus

SUBMITTER: Francesca Buffa

PROVIDER: E-GEOD-39413 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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A core human primary tumor angiogenesis signature identifies the endothelial orphan receptor ELTD1 as a key regulator of angiogenesis.

Masiero Massimo M Simões Filipa Costa FC Han Hee Dong HD Snell Cameron C Peterkin Tessa T Bridges Esther E Mangala Lingegowda S LS Wu Sherry Yen-Yao SY Pradeep Sunila S Li Demin D Han Cheng C Dalton Heather H Lopez-Berestein Gabriel G Tuynman Jurriaan B JB Mortensen Neil N Li Ji-Liang JL Patient Roger R Sood Anil K AK Banham Alison H AH Harris Adrian L AL Buffa Francesca M FM

Cancer cell 20130718 2

Limited clinical benefits derived from anti-VEGF therapy have driven the identification of new targets involved in tumor angiogenesis. Here, we report an integrative meta-analysis to define the transcriptional program underlying angiogenesis in human cancer. This approach identified ELTD1, an orphan G-protein-coupled receptor whose expression is induced by VEGF/bFGF and repressed by DLL4 signaling. Extensive analysis of multiple cancer types demonstrates significant upregulation of ELTD1 in tumo ...[more]

PMID: 23871637

Similar Datasets

Regulation of gene expressions in vivo by anti-VEGF and anti-Notch therapy [HG-U133_Plus_2]

Project description:U87-EV human glioblastoma xenograft tumours is therapeutically treated by bevacizumab, a humanized anti-human VEGF mAb, or dibenzazepine (DBZ), when tumour is established in BALB/c SCID mice. At the end point, collect tumour samples and extracted total RNA for microarray to investigate the gene profile changes compared to control. These include the genes from human tumour cells and mouse host stroma cells. 3 control samples, 3 dibenzazepine-treated samples, 3 bevacizumab-treated samples

2014-04-25 | E-GEOD-39223 | biostudies-arrayexpress

Regulation of gene expressions in vivo by anti-VEGF therapy

Project description:U87-EV human glioblastoma xenograft tumours is therapeutically treated by bevacizumab, a humanized anti-human VEGF mAb, when tumour is established in BALB/c SCID mice. At the end point, collect tumour samples and extracted total RNA for microarray to investigate the gene profile changes compared to control. These include the genes from human tumour cells and mouse host stroma cells. 3 control samples versus 3-bevacizumab treated samples

2014-04-25 | E-GEOD-37956 | biostudies-arrayexpress

Regulation of gene expressions in vivo by anti-VEGF and anti-Notch therapy [Mouse430_2]

Project description:U87-EV human glioblastoma xenograft tumours is therapeutically treated by bevacizumab, a humanized anti-human VEGF mAb, or dibenzazepine (DBZ) when tumour is established in BALB/c SCID mice. At the end point, collect tumour samples and extracted total RNA for microarray to investigate the gene profile changes compared to control. These include the genes from human tumour cells and mouse host stroma cells.

2014-04-25 | GSE39413 | GEO

Regulation of gene expressions in vivo by anti-VEGF and anti-Notch therapy [HG-U133_Plus_2]

2014-04-25 | GSE39223 | GEO

Transcription profiling by array of pancreatic cells from C57BL/6 mice following dibenzazepine treatment

Project description:DBZ (dibenzazepine) treatment in C57BL/6 mice, pancreatic gene expression

2007-12-31 | E-MEXP-1276 | biostudies-arrayexpress

TMT analysis of tissue proteomics in bevacizumab-resistant xenograft tumor tissuein nude mice

Project description:TMT proteomics was used to detect the difference in protein expression of bevacizumab-resistant xenograft tumor tissue in nude mice.

2022-10-13 | PXD030202 | Pride

Transcription profiling of mouse brain tissue from HtrA2 knockouts

Project description:Cellular stress responses can be activated following functional defects in organelles such as mitochondria and the endoplasmic reticulum. Mitochondrial dysfunction caused by loss of the serine protease HtrA2 leads to a progressive movement disorder in mice and has been linked to parkinsonian neurodegeneration in humans. Here we demonstrate that loss of HtrA2 results in transcriptional up-regulation of nuclear genes characteristic of the integrated stress response, including the transcription factor CHOP, selectively in the brain. We also show that loss of HtrA2 results in the accumulation of unfolded proteins in the mitochondria, defective mitochondrial respiration and enhanced production of reactive oxygen species that contribute to the induction of CHOP expression and to neuronal cell death. CHOP expression is also significantly increased in Parkinsonâs disease patientsâ brain tissue. We therefore propose that this brain-specific transcriptional response to stress may be important in the advance of neurodegenerative diseases. Experiment Overall Design: This experiment was set out to identify genes that are differentially expressed in brain tissue from the cortex of HtrA2 knockout (KO) mice compared to wild type (WT) littermates. We chose a cortical region since there is no evidence of neuronal loss in this region enabling us to compare mRNA transcripts in identical cellular populations. Brains of littermate WT and HtrA2 KO mice were dissected to obtain cortex tissue at post-natal day 29 (P29). RNA was isolated and samples were processed for hybridisation (6 samples in total, 3 replicates for each genotype).

2009-01-13 | E-GEOD-13033 | biostudies-arrayexpress

Transcription profiling of human xenografts produced from an endometrial cell line treated with bevacizumab (Avastin)

Project description:Microarrays were used to determine the efficacy of bevacizumab (a monoclonal antibody against the vascular endothelial growth factor and its receptors.) on endometrial cancer cells. Endometrial cancer is the most frequent gynecologic cancer in women. Long term outcomes for patients with advanced stage or recurrent disease are poor. Targeted molecular therapy against the vascular endothelial growth factor (VEGF) and its receptors constitute a new therapeutic option for these patients. The goal of our work was to assess the potential effectiveness of inhibition of VEGF/VEGFR signaling in a xenograft model of endometrial cancer using bevacizumab (Avastin, a humanized antibody against VEGFA). We also aimed to identify molecular markers of sensitivity or resistance to this agent. We show that bevacizumab retards tumor growth in athymic mice by inhibiting molecular components of signaling pathways that sustain cell survival and proliferation. We also demonstrate that resistance to bevacizumab may involve up-regulation of antiapoptotic genes and certain proto-oncogenes. Experiment Overall Design: Human xenografts produced from endometrial cell line, grown in athymic mice, were treated in vivo with bevacizumab.

2009-11-16 | E-GEOD-18195 | biostudies-arrayexpress

Transcription profiling of mouse embryonic fibroblasts from HtrA2 knockoutafter rotenone treatment. HtrA2 knockout mice have a movement disorder which may be similar to Parkinsons disease

Project description:Cellular stress responses can be activated following functional defects in organelles such as mitochondria and the endoplasmic reticulum. Mitochondrial dysfunction caused by loss of the serine protease HtrA2 leads to a progressive movement disorder in mice and has been linked to parkinsonian neurodegeneration in humans. Here we demonstrate that loss of HtrA2 results in transcriptional up-regulation of nuclear genes characteristic of the integrated stress response, including the transcription factor CHOP, selectively in the brain. We also show that loss of HtrA2 results in the accumulation of unfolded proteins in the mitochondria, defective mitochondrial respiration and enhanced production of reactive oxygen species that contribute to the induction of CHOP expression and to neuronal cell death. CHOP expression is also significantly increased in Parkinsonâs disease patientsâ brain tissue. We therefore propose that this brain-specific transcriptional response to stress may be important in the advance of neurodegenerative diseases. Experiment Overall Design: This experiment was set out to identify genes that are differentially regulated upon rotenone treatment in HtrA2 knockout (KO) mouse embryonic fibroblasts (MEFs) compared to wild type (WT) MEFs. Primary MEFs were isolated and at passage 4 subjected to treatment with vehicle (control) or 1 Î¼M rotenone (rot) for 4 hrs. 3 replicates were performed. RNA was isolated and samples were processed for hybridisation (12 samples in total).

2009-01-13 | E-GEOD-13034 | biostudies-arrayexpress

Transcription profiling of mouse HtrA2 knockout mice with a movement disorder (possible Parkinsons model) reveals mitochondrial dysfunction by loss of HtrA2 results in the activation of a brain-specific transcriptional stress response

Project description:Cellular stress responses can be activated following functional defects in organelles such as mitochondria and the endoplasmic reticulum. Mitochondrial dysfunction caused by loss of the serine protease HtrA2 leads to a progressive movement disorder in mice and has been linked to parkinsonian neurodegeneration in humans. Here we demonstrate that loss of HtrA2 results in transcriptional up-regulation of nuclear genes characteristic of the integrated stress response, including the transcription factor CHOP, selectively in the brain. We also show that loss of HtrA2 results in the accumulation of unfolded proteins in the mitochondria, defective mitochondrial respiration and enhanced production of reactive oxygen species that contribute to the induction of CHOP expression and to neuronal cell death. CHOP expression is also significantly increased in Parkinson’s disease patients’ brain tissue. We therefore propose that this brain-specific transcriptional response to stress may be important in the advance of neurodegenerative diseases. This SuperSeries is composed of the following subset Series:; GSE13033: Differentially expressed genes in brain tissue from HtrA2 knockout mice; GSE13034: Differentially regulated genes in HtrA2 knockout MEFs upon rotenone treatment Experiment Overall Design: Refer to individual Series

2008-12-05 | E-GEOD-13035 | biostudies-arrayexpress

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