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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 (I)

ABSTRACT: 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.

ORGANISM(S): Mus musculus

SUBMITTER: Antonina Mitrofanova

PROVIDER: E-GEOD-69211 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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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. 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-69213 | biostudies-arrayexpress

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.

2015-09-17 | GSE69211 | GEO

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

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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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EVALUATION IN A MOUSE PROSTATE CANCER XENOGRAFT MODEL OF THE EFFECTIVENESS OF CYCLOPHOSPHAMIDE METRONOMIC REGIMEN

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EVALUATION IN A MOUSE PROSTATE CANCER XENOGRAFT MODEL OF THE EFFECTIVENESS OF CYCLOPHOSPHAMIDE METRONOMIC REGIMEN

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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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The mTOR pathway is necessary for survival of mice with short telomeres.

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