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

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

PROVIDER: PRJNA701571 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13696700.fastq.gz	Fastqsanger.gz
	SRR13696701.fastq.gz	Fastqsanger.gz
	SRR13696682.fastq.gz	Fastqsanger.gz
	SRR13696683.fastq.gz	Fastqsanger.gz
	SRR13696684.fastq.gz	Fastqsanger.gz

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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

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

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

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

| PRJNA701570 | ENA

Genome-wide analysis of gene expression in VAV1-/- versus VAV1+/+ bone marrow (BM)-macrophages

Project description:Analysis of differential gene expression profiles in VAV1-/- versus VAV+/+ BM-macrophages , respectively. A distinct expression profile in VAV1-/- versus VAV1+/+ (wild-type) BM-macrophages allows to resolve molecular mechanisms. Total RNA was obtained froms BM-macrophages of VAV1+/+ and VAV1-/- mice

2013-03-08 | E-GEOD-36123 | biostudies-arrayexpress

Genome-wide analysis of gene expression in VAV1-/- versus VAV1+/+ bone marrow (BM)-macrophages

2013-03-08 | GSE36123 | GEO

EXPRESSION OF VAV1 IN GLIOBLASTOMA MULTIFORME

Project description:Background: Even though much progress has been made in the understanding of the molecular nature of glioma, the survival rates of patients affected of this tumour have not changed significantly during these years. Thus, a deeper understanding of this malignancy is still needed in order to predict its outcome and improve patient treatment. Here, we report that VAV1, a GDP/GTP exchange factor for Rho/Rac proteins with oncogenic potential that is involved in the regulation of cytoskeletal dynamics and cell migration. Methodology/Principal Findings: VAV1 is overexpressed in 32 patients diagnosed with high-grade glioma. Such overexpression is linked to the parallel upregulation of a number of genes coding for proteins also involved in cell invasion- and migration-related processes. Unexpectedly, immunohistochemical experiments revealed that VAV1 is not expressed in glioma cells. Instead, VAV1 is found in non-tumoral astrocyte-like cells that are located either peritumoraly or perivascularly, suggesting that its expression is linked to synergistic signalling cross-talk between cancer and infiltrating cells. Conclusions/Significance: Interestingly, we show that the pattern of expression of VAV1 is a good prognostic factor to unveil populations of high-grade glioma patients with different survival and progression free survival rates.

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Cancer-associated mutations in VAV1 trigger variegated signaling outputs and drive T cell lymphomagenesis

Project description:Mutations in VAV1, a multifunctional signaling protein essential for T lymphocytes, have been recently found in peripheral T cell lymphoma (PTCL) and other tumors. However, their pathobiological significance remains unsettled. Here, we show that these mutations belong to several subclasses according to the spectra of VAV1 signaling branches deregulated by them. These mutations target both known and new regulatory hotspots as well as transitional activation states of the protein. The most frequent VAV1 mutant subclass drives PTCL formation in mice by exacerbating normal VAV1- dependent signaling responses in follicular helper T cells.

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FYN-TRAF3IP2 activating fusion oncogene in peripheral T-cell lymphoma

Project description:FYN-TRAF3IP2 activating fusion oncogene in peripheral T-cell lymphoma

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Characterization of the spectrum of trivalent VAV1 mutation-driven tumors using a gene-edited mouse model

Project description:VAV1 mutations have been recently found in peripheral T cell lymphoma and non-small cell lung cancer. To understand their pathogenic potential, we generated a gene-edited mouse model that expresses a Vav1 mutant protein that recapitulates the signaling alterations present the VAV1 mutant subclass most frequently found in tumors. We could not detect any overt tumorigenic process in those mice. However, the concurrent elimination of the Trp53 tumor suppressor gene in them drives T cell lymphomagenesis. This process represents an exacerbation of the normal functions that wild-type Vav1 plays in follicular helper T cells. We also found that, in combination with an oncogenic Kras mutation, the Vav1 mutant version favors progression of non-small cell lung cancer. These data indicate that VAV1 mutations play critical, although highly cell typespecific roles in tumorigenesis. They also indicate that such functions are contingent on the mutational landscape of the tumors involved.

2022-10-12 | GSE189221 | GEO

Vav1 Promotes B-Cell Lymphoma Development.

Project description:Vav1 is normally and exclusively expressed in the hematopoietic system where it functions as a specific GDP/GTP nucleotide exchange factor (GEF), firmly regulated by tyrosine phosphorylation. Mutations and overexpression of Vav1 in hematopoietic malignancies, and in human cancers of various histologic origins, are well documented. To reveal whether overexpression of Vav1 in different tissues suffices for promoting the development of malignant lesions, we expressed Vav1 in transgenic mice by using the ubiquitous ROSA26 promoter (Rosa Vav1). We detected Vav1 expression in epithelial tissues of various organs including pancreas, liver, and lung. While carcinomas did not develop in these organs, surprisingly, we noticed the development of B-cell lymphomas. Rac1-GTP levels did not change in tissues from Rosa Vav1 mice expressing the transgenic Vav1, while ERK phosphorylation increased in the lymphomas, suggesting that signaling pathways are evoked. One of the growth factors analyzed by us as a suspect candidate to mediate paracrine stimulation in the lymphocytes was CSF-1, which was highly expressed in the epithelial compartment of Rosa Vav1 mice. The expression of its specific receptor, CSF-1R, was found to be highly expressed in the B-cell lymphomas. Taken together, our results suggest a potential cross-talk between epithelial cells expressing Vav1, that secrete CSF-1, and the lymphocytes that express CSF-1R, thus leading to the generation of B-cell lymphomas. Our findings provide a novel mechanism by which Vav1 contributes to tumor propagation.

| S-EPMC8946024 | biostudies-literature

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