LNCAP xenograft prostate cancer progression model in NOD-SCID mice
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PROVIDER: PRJNA872388 | ENA |
REPOSITORIES: ENA
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Project description:Xenografts are useful in vivo tumour models for investigating cancer progression, therapeutic responses and predicting anti-cancer drug response in patients with cancer of a similar phenotype. We have generated bulk RNA-seq data from LNCaP xenografts of a large and well-annotated prostate cancer progression study, investigating responsiveness and subsequent resistance to therapies targeting the androgen receptor (AR). LNCaP xenograft tumour establishment and initial growth are dependent on androgens in male mice (PRE-CX / pre-castration group). Upon castration, AR activity and tumour growth are suppressed (POST-CX / post-castration group), however, this initial responsiveness to castration reproducibly gives way to castration-resistance (CRPC / castration-resistant prostate cancer). Further treatment of CRPC with the AR targeting drug enzalutamide (ENZ) initially provides a therapeutic response (ENZ Sensitive; ENZS), however, resistance emerges in time (ENZ Resistant; ENZR).
2022-09-07 | GSE211856 | GEO
Project description:Introduction. Glucocorticoids are critical drugs used to treat acute lymphoblastic leukemia, and response to glucocorticoids is highly predictive of outcome. Here we report a study evaluating the NOD/SCID xenograft mouse model to investigate glucocorticoid-induced gene expression. Methods. NOD/SCID mice were inoculated with ALL-3, a glucocorticoid-sensitive xenograft, and when highly engrafted were randomised to either dexamethasone 15mg/kg or vehicle control IP. Cells were harvested at 0, 8, 24 or 48 hours thereafter, RNA was extracted and hybridised onto Illumina WG-6_V3 chips. Results. The 8 hour dexamethasone-treated timepoint had the highest number of significantly differentially expressed genes with minimal changes seen across the time-matched controls. Replicate analysis revealed that using data from 3 replicates instead of 4 resulted in excellent recovery scores of >0.9 at timepoints with high signal. When assessed at the level of pathways, gene expression changes in the 8 hour xenograft samples were similar to patients treated with glucocorticoids. Conclusions. The NOD/SCID xenograft mouse model provides a reproducible experimental model system in which to investigate clinically-relevant mechanisms of in vivo glucocorticoid-induced gene regulation in ALL; the 8 hour timepoint provides the highest number of significantly differentially expressed genes; time-matched controls are redundant and excellent recovery scores can be obtained with 3 replicates. At 0, 8, 24 or 48 hours, NOD/SCID xenograft mice were treated with vehicle control, or dexamethasone. We used 4 biological replicates per time point (3 at the 48hour time point), each of which went onto an Illumina HumanWG-6_V3_0_R1_11282955_A microarray. Samples from each of the 7 groups were divided across a total of 5 microarray slides
2011-11-28 | E-GEOD-30392 | biostudies-arrayexpress
Project description:Introduction. Glucocorticoids are critical drugs used to treat acute lymphoblastic leukemia, and response to glucocorticoids is highly predictive of outcome. Here we report a study evaluating the NOD/SCID xenograft mouse model to investigate glucocorticoid-induced gene expression. Methods. NOD/SCID mice were inoculated with ALL-3, a glucocorticoid-sensitive xenograft, and when highly engrafted were randomised to either dexamethasone 15mg/kg or vehicle control IP. Cells were harvested at 0, 8, 24 or 48 hours thereafter, RNA was extracted and hybridised onto Illumina WG-6_V3 chips. Results. The 8 hour dexamethasone-treated timepoint had the highest number of significantly differentially expressed genes with minimal changes seen across the time-matched controls. Replicate analysis revealed that using data from 3 replicates instead of 4 resulted in excellent recovery scores of >0.9 at timepoints with high signal. When assessed at the level of pathways, gene expression changes in the 8 hour xenograft samples were similar to patients treated with glucocorticoids. Conclusions. The NOD/SCID xenograft mouse model provides a reproducible experimental model system in which to investigate clinically-relevant mechanisms of in vivo glucocorticoid-induced gene regulation in ALL; the 8 hour timepoint provides the highest number of significantly differentially expressed genes; time-matched controls are redundant and excellent recovery scores can be obtained with 3 replicates.
2011-11-28 | GSE30392 | GEO
Project description:We overexpressed the long non-coding RNA GHSROS in the metastatic prostate cancer cell line LNCaP and subcutaneously injected the cells into NOD/SCID mice.
2019-11-14 | GSE103320 | GEO
Project description:Prostate Cancer Stem Cells (CSCs) are considered one of the main reasons the tumor recurrence after chemotherapy. Here we employed a chemoresistant xenograft prostate cancer model in NOD/SCID mice and found CD54 is a reliable new marker for prostate CSCs. Gene expression profile were utilized to analyze stemness-related genes in cancer stem cells. 12 Male NOD/SCID mice were obtained from the Animal Center of the Chinese Academy of Medical Science (Beijing, China). For xenograft generation, 1Ã106 LNCaP cells were subcutaneously injected into the backs of NOD/SCID mice (n=24). When tumors reached a diameter of 5 mm after 3 d, mice were randomly divided into two groups without castration (12 per group). Mice in the treatment group were administered with cisplatin at a dose of 5 mg/kg every 3 d for 30 d. Mice in the control group were treated with vehicle PBS. Tumors were taken out for microarray assay after 30 d.
2016-02-23 | E-GEOD-78196 | biostudies-arrayexpress
Project description:Prior to the onset of autoimmune destruction, type 1 diabetic patients and an animal model thereof, the nonobese diabetic (NOD) mouse, show morphological and functional abnormalities in target organs, which may act as inciting events for leukocyte infiltration. To better understand these abnormalities, but without the complications associated with inflammatory infiltrates, we examined genes expressed in autoimmune target tissues (pancreas, submandibular glands, and lacrimal glands) of NOD/scid mice and of autoimmune-resistant C57BL6/scid mice. Keywords: tissue expression, disease prone versus resistant strain comparison
2006-07-07 | GSE4953 | GEO
Project description:We report the single-cell transcriptome of breast cancer stem cells (BCSCs) from solid tumors taken from NOD/SCID mice.
2019-10-25 | GSE124888 | GEO
Project description:Glioblastoma cell lines were xenografted onto mice and resulting tumors were profiled by microarray. Xenograft recipient mice were NOD/SCID/gamma (NSG) male mice 3 months old.
2013-07-01 | GSE46028 | GEO
Project description:Prior to the onset of autoimmune destruction, type 1 diabetic patients and an animal model thereof, the nonobese diabetic (NOD) mouse, show morphological and functional abnormalities in target organs, which may act as inciting events for leukocyte infiltration. To better understand these abnormalities, but without the complications associated with inflammatory infiltrates, we examined genes expressed in autoimmune target tissues (pancreas, submandibular glands, and lacrimal glands) of NOD/scid mice and of autoimmune-resistant C57BL6/scid mice. Experiment Overall Design: Pancreata (6 weeks old mice), submandibular (9 and 15 weeks), and lacrimal glands (15 weeks) from individual NOD-scid and B6-scid mice were isolated for RNA extraction and hybridization on Affymetrix microarrays.
2007-11-29 | E-GEOD-4953 | biostudies-arrayexpress
Project description:To identify molecular singnal alterations between androgen dependent prostate cancer and castration resistant prostate cancer, we performed interspecies comparative microarray analyses using RNAs prepared from uncastrasion and castration tumor from LNCAP Orhotopic xenograft models of prostate cancer. microarray data from uncastrasion and castration tumor revealed that the gene expression profile is most significantly altered in between androgen dependent prostate cancer and castration resistant prostate cancer. Comparative analyses of LNCAP Orhotopic xenograft models of prostate cancer showed that genes involved in androgen dependent and androgen independent tumor were significantly altered.
2013-04-20 | GSE46218 | GEO