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Chromosomal deletions linked to p53 loss of heterozygosity promote cancer through p53-independent mechanisms

ABSTRACT: The purpose of current study is to identify the differentiated gene expression associated with mouse 11B3 deletion, syntenic to human chromosome 17p13.1. We compared four different mouse acute myeloid leukemia cells, freshly isolated from mouse bone marrows with either 11B3fl/p53fl;shNf1;shMll3;Vav1-Cre or p53fl/fl;shNf1;shMll3;Vav1-Cre. The RNA-seq results indicate that genes located on chromosome 11B3 mostly reduce gene expression level in 11B3 deleted leukemia cells.

ORGANISM(S): Mus musculus

PROVIDER: GSE69654 | GEO | 2016/04/04

SECONDARY ACCESSION(S): PRJNA286105

REPOSITORIES: GEO

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Chromosomal deletions linked to p53 loss of heterozygosity promote cancer through p53-independent mechanisms

Project description:The purpose of current study is to identify the differentiated gene expression associated with mouse 11B3 deletion, syntenic to human chromosome 17p13.1. We compared four different mouse acute myeloid leukemia cells, freshly isolated from mouse bone marrows with either 11B3fl/p53fl;shNf1;shMll3;Vav1-Cre or p53fl/fl;shNf1;shMll3;Vav1-Cre. The RNA-seq results indicate that genes located on chromosome 11B3 mostly reduce gene expression level in 11B3 deleted leukemia cells. Examination RNA expression level in 11B3-deleted vs p53-loss only samples.

2016-04-04 | E-GEOD-69654 | biostudies-arrayexpress

CU44_WGS of YFP+ sorted tumor cells from murine PKCY and A3A_PKCY pancreatic tumors

Project description:We aimed to decipher human APOBEC3A driven genomic differences in pancreatic tumors in vivo using a genetically engineered mouse model for pancreatic cancer. Murine pancreatic tumor formation was driven by p53fl/+;KrasLSL-G12D/+;Pdx1-Cre;Rosa26LSL-YFP (PKCY) and p53fl/+;KrasLSL-G12D/+;Pdx1-Cre; Rosa26LSL-YFP; A3A+/- (A3A PKCY).

2021-09-06 | E-MTAB-9843 | biostudies-arrayexpress

RS8_RNA-seq of murine PKCY and A3A_PKCY pancreatic tumors

Project description:We aimed to decipher human APOBEC3A driven transcriptomic differences in pancreatic tumors in vivo using a genetically engineered mouse model for pancreatic cancer. Murine pancreatic tumor formation was driven by p53fl/+;KrasLSL-G12D/+;Pdx1-Cre;Rosa26LSL-YFP (PKCY) and p53fl/+;KrasLSL-G12D/+;Pdx1-Cre; Rosa26LSL-YFP; A3A+/- (A3A PKCY).

2021-09-06 | E-MTAB-9966 | biostudies-arrayexpress

CU37_WES of paired murine PKCY and A3A PKCY tumors and normal tissue

Project description:We aimed to decipher human APOBEC3A driven mutational differences in pancreatic tumor in vivo using a genetically engineered mouse model of pancreatic cancer. Murine pancreatic tumor formation was driven by p53fl/+;KrasLSL-G12D/+;Pdx1-Cre;Rosa26LSL-YFP (PKCY) and p53fl/+;KrasLSL-G12D/+;Pdx1-Cre; Rosa26LSL-YFP; A3A+/- (A3A PKCY).

2021-09-06 | E-MTAB-9972 | biostudies-arrayexpress

Heterozygous and Homozygous Knock-Out of USP7 mouse models [mouse_RNA-seq]

Project description:RNAseq analysis of USP7 conditional knock-out (cKO) mice. They were designed to flox exon 6 of USP7 and to allow deletion of exon 6 upon expression of Cre recombinase 27. USP7FL/FL mice were bred with Vav1-Cre mice to obtain USP7FL/wt-Vav1-Cre mice (heterozygote). USP7FL/FL-Vav1-Cre mice (homozygote) were obtained via breeding of heterozygous cKO mice.

2021-03-09 | GSE148521 | GEO

Single cell RNA-seq analysis of normal, premalignant state and tumor mouse models of VAV1-MYOF gene fusion in Peripheral T-Cell Lymphoma

Project description:The goal of this study is to identify transcriptomic effects of VAV1-MYOF expression in mouse CD4+ T lymphocytes and tumor progression in TET2KO and TET2WT backgrounds. To this end, mice conditionally expressing VAV1-MYOF were crossed with the CD4CreERT2 line or CD4-Cre, under the control of the mouse Cd4 promoter to generate CD4 specific VAV1-MYOF models. In inducible models, mice were treated with vehicle only or Tamoxifen to induce expression of VAV1-MYOF1 in CD4+ T cells. Mice were crossed with CD4-CreERT2 Tet2f/f to obtain the experimental phenotypes. Whole spleen samples were processed and single cell suspensions were analyzed using scRNA-seq technologies.

2021-05-12 | GSE166672 | GEO

RNA Sequencing Quantitative Analysis of cell lines derived from tumours from two mouse models of human osteosarcoma that recapitulate clinically distinct human osteosarcoma subtypes.

Project description:Purpose: Osteosarcoma (OS) is the most common primary bone malignancy. OS consists of several subtypes including fibroblastic, osteoblastic and chondroblastic OS. We have developed genetically engineered mouse models of human OS that recapitulate two distinct subtypes, fibroblastic (Osx-CreLox p53-/- Rb-/-) and osteoblastic (Osx-Cre shRNA p53-/-) OS. The goal of this study was to identify transcriptional differences that distinguish the two subtypes. Methods: mRNA profiles of cell lines derived from tumours from Osx-Cre p53fl/fl Rbfl/fl (fibroblastic OS) and Osx-Cre shRNA TRE-p53.1224 pRbfl/fl (osteoblastic OS) mouse models were generated by RNA sequencing, in triplicate, using Illumina HiSeq2000. The sequence reads that passed quality filters were analyzed at the transcript level with TopHat followed by Cufflinks. Results: Using an optimized data analysis workflow, we mapped about 30 million sequence reads per sample to the mouse genome (build mm9) and identified 12,436 transcripts in the tumours of Osx-Cre p53fl/fl Rbfl/fl and 12,074 Osx-Cre shRNA TRE-p53.1224 pRbfl/fl with the TopHat workflow. RNA-seq data confirmed stable expression of 25 known housekeeping genes. Conclusions: Our study represents a detailed analysis of OS subtype transcriptomes generated by RNA-seq technology. mRNA profiles of cell lines derived from tumours from two genetically engineered mouse models of human osteosarcoma (Osx-Cre p53fl/fl Rbfl/fl and Osx-Cre shRNA TRE-p53.1224 pRbfl/fl) were generated by deep sequencing, in triplicate, using Illumina HiSeq 2000.

2015-07-06 | E-GEOD-58916 | biostudies-arrayexpress

Wnt inhibitory factor 1 (WIF1) is a marker of osteoblastic differentiation stage and is not silenced by DNA methylation in osteosarcoma

Project description:Purpose: We have used microarrays to identify gene expression profiles that distinguish mouse OS cells from normal pre-osteoblast cells and mature osteoblast cells. Methods: Transcriptional profiles of three cell lines derived from tumors from Osx-Cre p53fl/fl Rbfl/fl (fibroblastic OS) mouse model, and from pre-osteoblast cells (Kusa4b10 mouse bone marrow stromal cell line) and osteoblast cells (derived by in vitro differentiation of the Kusab410 mouse bone marrow stromal cell line) were generated by microarray analysis, each in triplicate, using Affymetrix mouse Gene1.0ST arrays. Transcriptional profiles were analyzed in cell lines derived from tumors from a genetically engineered mouse model of human osteosarcoma (Osx-Cre p53fl/fl Rbfl/fl) and osteoblast cells derived from the Kusa4b10 mouse bone marrow stromal cell line, in the undifferentiated state (pre-osteoblasts) and differentiated state (osteoblasts).

2015-01-29 | E-GEOD-63939 | biostudies-arrayexpress

Stromal STAT5-mediated trophic activity regulates hematopoietic multipotent progenitor niche factors

Project description:Signal transducer and activator of transcription 5 (STAT5a and STAT5b) are intrinsically critical for normal hematopoiesis but are also expressed in stromal cells. However, hematopoiesis-supporting stromal function has not been reported. Here, STAT5ab knockout (KO) was generated with a variety of bone marrow hematopoietic and stromal Cre transgenic mouse strains. Pan-hematopoietic deletion with Vav1-Cre was the positive control for loss of multipotent hematopoietic function but surprisingly dysregulated niche factor mRNA expression and deleted STAT5ab in CD45neg cells. Single cell transcriptome analysis of mouse bone marrow from wild-type or Vav1-Cre KO mice showed major changes in hematopoietic stem cell myeloid commitment genes and upregulated protein translation genes throughout myeloid-primed clusters.

2023-10-01 | GSE214857 | GEO

Bulk transcriptomic analysis of normal, premalignant state and tumor mouse models of VAV1-MYOF gene fusion in Peripheral T-Cell Lymphoma

Project description:The goal of this study is to identify transcriptomic effects of VAV1-MYOF expression in mouse CD4+ T lymphocytes in tumor development as well as changes in the microenvironment. To this end, mice conditionally expressing VAV1-MYOF were crossed with the CD4CreERT2 line or CD4-Cre, under the control of the mouse Cd4 promoter to generate CD4 specific VAV1-MYOF models. In inducible models, mice were treated with vehicle only or Tamoxifen to induce expression of VAV1-MYOF1 in CD4+ T cells. CD4CreERT2 mice were included as a negative control. Total RNA was extracted from whole spleen samples or CD4+ T cells isolated by single cell suspensions of spleen by negative selection using the mouse naive CD4+ T Cell Isolation Kit (Milteny#130-104-453) according to the manufacturer’s protocol. Standard Illumina poly-A RNA seq was performed.

2021-05-12 | GSE166671 | GEO

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