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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Predicting drug response in human prostate cancer from preclinical analysis of in vivo mouse models (II)

ABSTRACT: Analysis of the transcriptome of allografted mouse tumors after treatment with rapamycin and PD0325901. Nkx3.1CreERT2/+; Ptenflox/flox; KrasLSL-G12D/+ (NPK mice) were induced and their tumors removed to generate allograft lines by implanting a 1.5 mm3 tumor fragment in the subcutaneous space of athymic nude mice. Allografted NPK tumors were allowed to grow until they reached a volume of 1 cm3, at which moment they were randomly assigned to either vehicle (Veh) or combination therapy using rapamycin and PD0325901 (RAPPD). Allografted mice were administered rapamycin (10 mg/kg) and PD0325901 (10 mg/kg) during five consecutive days (Allo SHORT). Mice were euthanized in the fifth day 6 hours after having received the last treatment and the tumors were harvested and snap frozen for subsequent molecular analysis. Total RNA obtained from prostate tumors/tissues. Prostate tumors/tissues were harvested and processed for RNA isolation and transcriptome analysis using the MagMAX RNA isolation kit (Ambion). Total RNA was amplified and labelled for subsequent microarrays hybridization using the Illumina TotalPrep RNA Amplification Kit.

ORGANISM(S): Mus musculus

SUBMITTER: Antonina Mitrofanova

PROVIDER: E-GEOD-69213 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Predicting drug response in human prostate cancer from preclinical analysis of in vivo mouse models (I)

Project description:Analysis of the transcriptome of mouse models of prostate cancer after treatment with rapamycin and PD0325901 combination therapy or standard of care docetaxel. The Nkx3.1CreERT2/+; Ptenflox/flox; KrasLSL-G12D/+ (NPK mice) was used in this study. Two months after tumor induction, mice were randomly assigned to vehicle (Veh) or treatments groups, such as rapamycin and PD0325901 (RAPPD) or docetaxel (Docetaxel). For the treatment groups mice were administered rapamycin (10 mg/kg) and PD0325901 (10 mg/kg) or docetaxel (10 mg/kg) for 5 days (SHORT) or for 1 month (LONG). At the end of the treatment, mice were euthanized, tumors harvested and snap frozen for subsequent molecular analysis. Total RNA obtained from prostate tumors/tissues. Prostate tumors/tissues were harvested and processed for RNA isolation and transcriptome analysis using the MagMAX RNA isolation kit (Ambion). Total RNA was amplified and labelled for subsequent microarrays hybridization using the Illumina TotalPrep RNA Amplification Kit.

2015-09-17 | E-GEOD-69211 | biostudies-arrayexpress

Predicting drug response in human prostate cancer from preclinical analysis of in vivo mouse models (II)

Project description:Analysis of the transcriptome of allografted mouse tumors after treatment with rapamycin and PD0325901. Nkx3.1CreERT2/+; Ptenflox/flox; KrasLSL-G12D/+ (NPK mice) were induced and their tumors removed to generate allograft lines by implanting a 1.5 mm3 tumor fragment in the subcutaneous space of athymic nude mice. Allografted NPK tumors were allowed to grow until they reached a volume of 1 cm3, at which moment they were randomly assigned to either vehicle (Veh) or combination therapy using rapamycin and PD0325901 (RAPPD). Allografted mice were administered rapamycin (10 mg/kg) and PD0325901 (10 mg/kg) during five consecutive days (Allo SHORT). Mice were euthanized in the fifth day 6 hours after having received the last treatment and the tumors were harvested and snap frozen for subsequent molecular analysis.

2015-09-17 | GSE69213 | GEO

Predicting drug response in human prostate cancer from preclinical analysis of in vivo mouse models (I)

2015-09-17 | GSE69211 | GEO

ETV4 promotes metastasis in response to combined activation of PI3kinase and RAS signaling in a mouse model of advanced prostate cancer

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2013-07-23 | E-GEOD-47697 | biostudies-arrayexpress

Cross-species analysis of genome-wide regulatory networks identifies a synergistic dependency between FOXM1 and CENPF that drives prostate cancer malignancy

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Genetic deletion of osteopontin in TRAMP mice enhances the growth of aggressive prostate cancer with feature of human neuroendocrine tumors

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2016-01-20 | E-GEOD-69903 | biostudies-arrayexpress

B-Raf activation cooperates with PTEN loss to drive c-Myc expression in advanced prostate cancer

Project description:Anaysis of the response to different therapeutic agents at the transcriptional level. The design of the experiment allows to determine how the comnination target therapy (Rapamycin + PD0325901) treatment shifted the transcriptome towards a less aggressive or even a wild type phenotype. It also allows exploring the molecular changes involved in the transition from a non metastatic to a metastatic prostate cancer mouse model. Total RNA obtained form vehicle treated Nkx3.1CE2/+; Ptenf/f; BrafCA/+ (n=3), combinatorial Rapamycin and PD0325901 treated Nkx3.1CE2/+; Ptenf/f; BrafCA/+ (n=3) and vehicle treated intact Nkx3.1CE2/+; Ptenf/f (n = 6) prostate. Please contact Cory Abate-Shen (cabateshen@columbia.edu) and Jingqiang Wang (jw2639@columbia.edu) for questions about the submission.

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Targeting resistance to Smoothened antagonists by inhibiting the PI3K pathway

Project description:This SuperSeries is composed of the following subset Series: GSE22005: Medulloblastoma tumors derived from Ptch+/-HIC+/- transgenic mouse allografted in nude mice GSE22006: Medulloblastoma tumors derived from Ptch+/-p53-/- transgenic mouse allografted in nude mice Refer to individual Series

2010-09-29 | E-GEOD-22007 | biostudies-arrayexpress

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