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The IL6Myc mouse is an immunocompetent model for the development of aggressive multiple myeloma (MM) [cell line RNA-seq]

ABSTRACT: The IL6Myc mouse is an immunocompetent model for the development of aggressive multiple myeloma (MM) [cell line RNA-seq]

PROVIDER: PRJNA911729 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22708040_1.fastq.gz	Fastqsanger.gz
	SRR22708040_2.fastq.gz	Fastqsanger.gz
	SRR22708041_1.fastq.gz	Fastqsanger.gz
	SRR22708041_2.fastq.gz	Fastqsanger.gz
	SRR22708042_1.fastq.gz	Fastqsanger.gz

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The IL6Myc mouse is an immunocompetent model for the development of aggressive multiple myeloma (MM) [cell line RNA-seq]

Project description:Multiple Myeloma (MM) is a neoplasm of plasma cells originating in the bone marrow and is the second most common blood cancer in the United States. One challenge in understanding the pathogenesis of Multiple Myeloma (MM) and improving treatment is a lack of immunocompetent mouse models. We previously developed the IL6Myc mouse that generates plasmacytomas at 100% frequency that phenotypically resemble aggressive MM. Using comprehensive genomic analysis, we found that the RNA expression patterns between tumors were somewhat heterogenous, but nonetheless resembled MMSET (multiple myeloma SET domain), an aggressive form of human myeloma with poor prognosis. Cell lines derived from the mouse tumors expressed cell-surface markers typical of MM, but also expressed BAFF-R, which is infrequently found in human MM. The cell lines also had heterogeneous responses to chemotherapeutic drugs typically used to treat human MM. Interestingly IL6Myc tumors accumulated variants in genes like those seen in human MM, as well as recurrent Ig translocations, a common characteristic of human MM. These data indicate that the IL6Myc model is a useful model for aggressive MM that can be used to develop treatment and understand how early myc expression influences disease etiology.

2023-12-06 | GSE220823 | GEO

The IL6Myc mouse is an immunocompetent model for the development of aggressive multiple myeloma (MM) [WES]

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The IL6Myc mouse is an immunocompetent model for the development of aggressive multiple myeloma (MM) [tumor RNA-seq]

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The IL6Myc mouse is an immunocompetent model for the development of aggressive multiple myeloma (MM)

Project description:The IL6Myc mouse is an immunocompetent model for the development of aggressive multiple myeloma (MM)

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The IL6Myc mouse is an immunocompetent model for the development of aggressive multiple myeloma (MM) [WES]

Project description:The IL6Myc mouse is an immunocompetent model for the development of aggressive multiple myeloma (MM) [WES]

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The IL6Myc mouse is an immunocompetent model for the development of aggressive multiple myeloma (MM) [tumor RNA-seq]

Project description:The IL6Myc mouse is an immunocompetent model for the development of aggressive multiple myeloma (MM) [tumor RNA-seq]

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Expression data of newly diagnosed multiple myeloma and extramedullary myeloma

Project description:Despite the development of novel therapeutic agents, multiple myeloma (MM) remains incurable, owing mainly to inevitable relapse in almost all patients. Some relapses occur as extramedullary disease (EMD), which is rare but is the most aggressive event in MM patients. Extramedullary myeloma (EMM) has extraordinary heterogeneous biological and clinical features. Previous studies have shown that expression levels of LncRNAs and mRNAs in different stages of MM are different. This study analyzes the expression levels of LncRNAs and mRNAs in primary plasma cells (PCs) from MM and EMM patients.

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MAQC-II Project: Multiple myeloma (MM) data set

Project description:The multiple myeloma (MM) data set (endpoints F, G, H, and I) was contributed by the Myeloma Institute for Research and Therapy at the University of Arkansas for Medical Sciences (UAMS, Little Rock, AR, USA). Gene expression profiling of highly purified bone marrow plasma cells was performed in newly diagnosed patients with MM. The training set consisted of 340 cases enrolled on total therapy 2 (TT2) and the validation set comprised 214 patients enrolled in total therapy 3 (TT3). Plasma cells were enriched by anti-CD138 immunomagnetic bead selection of mononuclear cell fractions of bone marrow aspirates in a central laboratory. All samples applied to the microarray contained more than 85% plasma cells as determined by 2-color flow cytometry (CD38+ and CD45-/dim) performed after selection. Dichotomized overall survival (OS) and eventfree survival (EFS) were determined based on a two-year milestone cutoff. A gene expression model of high-risk multiple myeloma was developed and validated by the data provider and later on validated in three additional independent data sets.

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Project description:One of the hallmarks of multiple myeloma (MM) is a permissive BM microenvironment. Increasing evidence suggest that cell-to-cell communication between myeloma and immune cells via tumor cell-derived extracellular vesicles (EV) plays a key role in the pathogenesis of MM. Hence, we aimed to explore BM immune alterations induced by MM-derived EV. For this, we inoculated immunocompetent BALB/cByJ mice with a myeloma cell line - MOPC315.BM -, inducing a MM phenotype. Upon tumor establishment, characterization of the BM microenvironment revealed the expression of both activation and suppressive markers by lymphocytes, such as Granzyme b and PD-1, respectively. In addition, conditioning of the animals with MOPC315.BM-derived EV, before transplantation of the MOPC315.BM tumor cells, did not anticipate the disease phenotype. However, it induced features of suppression in the BM milieu, such as an increase in PD-1 expression by CD4+ T cells. Overall, our findings reveal the involvement of MOPC315.BM-derived EV protein content as promoters of immune niche remodeling, strengthening the importance of assessing the mechanisms by which MM may impact the immune microenvironment.

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Project description:Multiple myeloma (MM) is an aggressive malignancy characterized by terminally differentiated plasma cells accumulation in the bone marrow (BM). MM BM exhibits elevated MΦs (macrophages) numbers relative to healthy BM. Here, we found that BMI1 modulates the pro-myeloma functions of MM-MΦs. We generated MΦs and MM-MΦs in vitro from wild type and BMI1-KO mice bone marrow. Total RNA was extracted using TRI reagent (MRC, Cat No.TR 118,USA) from flow sorted CD11b+ F4/80+ cells from murine BM-derived MΦs and MM-MΦs. Libraries were prepared using the VAHTSTM total RNA-seq library prep Kit for IIumina (Vazyme, Cat No. NR603, China). RNA-seq was performed by GENEWIZ (Suzhou, China) on an Illumina Hiseq platform.

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