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TrkA^WT NOD-Scid and TrkA^F592A NOD-Scid xenograft osteosarcoma (orthotopic) implants at 12 d post-143B OS cell innoculation for scRNA-Seq.

ABSTRACT: TrkA^WT NOD-Scid and TrkA^F592A NOD-Scid xenograft osteosarcoma (orthotopic) implants at 12 d post-143B OS cell innoculation for scRNA-Seq.

PROVIDER: PRJNA1061471 | ENA |

REPOSITORIES: ENA

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TrkA^WT;NOD-Scid and TrkA^F592A;NOD-Scid xenograft osteosarcoma (orthotopic) implants at 12 d post-143B OS cell innoculation for scRNA-Seq.

Project description:Bone pain is a presenting feature of osteosarcoma (OS) mediated by skeletal-innervating peripheral afferent neurons. Potential regulatory roles of skeletal-innervating neurons in OS beyond pain sensation are unknown. Here, a chemical-genetic approach was utilized to perturb innervation during osteosarcoma growth and disease progression. TrkA inhibition in transgenic mice led to a significant reduction in sarcoma-associated innervation and vascularization, tumor growth, and metastasis, and prolonged overall survival. Single-cell transcriptomics showed that chemical denervation led to prominent dysregulations in neurotrophin and BMP signaling among sarcoma cells, as well as VEGF signaling within tumor-associated endothelial cells. The importance of sarcoma innervation and neural-sarcoma crosstalk was further confirmed using human OS samples and sequencing datasets. In a translational effort, chemical inhibition of peripheral nerve growth via FDA-approved bupivacaine liposomes both alleviated tumor-associated bone and significantly delayed tumor growth. In sum, TrkA-expressing peripheral neurons positively regulate OS progression and neural inhibition appears to disrupt neurovascular coupling within the sarcoma leading to significantly reduced tumor growth and improved disease progression. These data suggest that interventions to prevent pathological innervation of osteosarcoma may represent a novel adjunctive therapy to improve clinical management.

2025-01-04 | GSE252589 | GEO

Expression data from NOD-scid vs B6-scid pancreas, submandibular glands, & lacrimal glands

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

Single-cell RNA sequencing of BCSCs from solid tumors taken from NOD/SCID mice

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

Transcription profiling of pancreata, submandibular, and lacrimal glands from NOD-scid and C57Bl/6-scid mice to study the gene expression patterns of nonobese diabetic mice.

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

scRNAseq of islets extracted from NOD-SCID mice shows no evidence for non-endocrine origin of regenerated beta cells

Project description:Single cell RNA sequencing was performed on adult NOD-SCID mice to identify the various cell types in the pancreatic islets of Langerhans

2023-03-15 | GSE225739 | GEO

LNCAP xenograft prostate cancer progression model in NOD-SCID mice

Project description:LNCAP xenograft prostate cancer progression model in NOD-SCID mice

| PRJNA872388 | ENA

T-cell acute lymphobalstic leukemia xenografts in NOD/SCID mouse

Project description:T-cell acute lymphobalstic leukemia xenografts in NOD/SCID mouse

| PRJNA643797 | ENA

Characterization of spleen Z cells from naïve NOD-SCID mouse

Project description:Eight NOD-SCID mice of 6-8 weeks old were sacrificed, and spleen cells harvested. Z cells were isolated using a red fluorescent TMR-Zfra peptide in cell sorting (Oncotarget. 2015 Feb 28;6(6):3737-51). Two cell populations were isolated, which are Z(-) and Z(+) cells, or designated as ZM for negative cells and ZP for positive cells. Mouse OneArray chips (Phalanx Biotech, Inc) were used for gene expression profiling. The goal of this research is to determine the specific gene expression profile in newly isolated spleen Z cells.

2017-05-02 | GSE98409 | GEO

Expression data from MDA-MB-231 derived tumors grown in NOD/SCID mice: control- and Memo1-targeted shRNA pools

Project description:0.5 x10^6 MDA-MB-231 cells, infected with lentivirus encoding either a control shRNA (shLacZ) or a shRNA targeting human Memo1, were injected into the second mammary fatpad of 6-8 week old female NOD/SCID mice and collected 4 weeks after injection.

2015-01-23 | GSE43672 | GEO

The NOD/SCID Xenograft Model Provides Clinically-Relevant Insights into Glucocorticoid-Induced Gene Expression in Childhood B-Cell Precursor Acute Lymphoblastic Leukemia

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

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