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ABSTRACT: Mouse model of human MYD88L265P mutation

PROVIDER: PRJNA560216 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9966560_1.fastq.gz	Fastqsanger.gz
	SRR9966560_2.fastq.gz	Fastqsanger.gz
	SRR9966554_1.fastq.gz	Fastqsanger.gz
	SRR9966554_2.fastq.gz	Fastqsanger.gz
	SRR9966555_1.fastq.gz	Fastqsanger.gz

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Transcriptional profiling of Myd88 L252P germinal center B-cells

Project description:A third of patients with diffuse large B-cell lymphoma (DLBCL) present with extranodal dissemination, which is associated with inferior clinical outcomes. MYD88L265P is a hallmark extranodal DLBCL mutation that supports lymphoma proliferation. Yet extranodal lymphomagenesis and the role of MYD88L265P in transformation remain mostly unknown. Here, we show that B cells expressing Myd88L252P (MYD88L265P murine equivalent) activate, proliferate, and differentiate with minimal T-cell costimulation. Additionally, Myd88L252P skewed B cells toward memory fate. Unexpectedly, the transcriptional and phenotypic profiles of B cells expressing Myd88L252P, or other extranodal lymphoma founder mutations, resembled those of CD11c+T-BET+ aged/autoimmune memory B cells (AiBC). AiBC-like cells progressively accumulated in animals prone to develop lymphomas, and ablation of T-BET, the AiBC master regulator, stripped mouse and human mutant B cells of their competitive fitness. By identifying a phenotypically defined prospective lymphoma precursor population and its dependencies, our findings pave the way for the early detection of premalignant states and targeted prophylactic interventions in high-risk patients.

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MYD88 L265P differential expression analysis

Project description:The wider transcriptional effects of MYD88L265P were explored by analysing the microarray datasets using the limma package. We focussed on evidence for differential expression between Myd88L265P and Card11L232LI transduced B cells because both cell populations were actively proliferating at the time of RNA isolation. When the transcriptome of MYD88L265P expressing B cells was compared with empty vector-expressing B cells using limma, 111 genes had strong evidence for differential expression with 88 increased in MYD88L265P cells. Compared to CARD11L232LI expressing B cells, 84 genes had strong evidence for differential expression in MYD88L265P B cells with 30 increased, including the plasma cell induced genes Prdm1 and Igj.

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Pre-neoplastic somatic mutations including MYD88L265P in lymphoplasmacytic lymphoma [scRNA-seq]

Project description:Normal-cell counterparts of solid and myeloid tumors accumulate mutations years before disease onset; whether this occurs in B-lymphocytes prior to lymphoma remains uncertain. We sequenced multiple stages of the B-lineage in elderly individuals and patients with lymphoplasmacytic lymphoma, a singular disease for studying lymphomagenesis because of high-prevalence of mutated MYD88. We observed similar accumulation of random mutations in B-lineages from both cohorts and, unexpectedly, found MYD88L265P in normal precursor and mature B-lymphocytes from lymphoma patients. We uncovered genetic and transcriptional pathways driving malignant transformation and leveraged these to model lymphoplasmacytic lymphoma in mice, based on mutated MYD88 in B-cell precursors and BCL2 overexpression. Thus, MYD88L265P is a pre-neoplastic event, which challenges current understanding of lymphomagenesis and may have implications for early detection of B-cell lymphomas.

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