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The genomic landscape of VkMYC myeloma highlights shared pathways of transformation between mice and humans
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The genomic landscape of VkMYC myeloma highlights shared pathways of transformation between mice and humans
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Journal Article
The genomic landscape of VkMYC myeloma highlights shared pathways of transformation between mice and humans
2024
Overview
Multiple myeloma (MM) is a heterogeneous disease characterized by frequent MYC translocations. Sporadic MYC activation in the germinal center of genetically engineered Vk*MYC mice is sufficient to induce plasma cell tumors in which a variety of secondary mutations are spontaneously acquired and selected over time. Analysis of 119 Vk*MYC myeloma reveals recurrent copy number alterations, structural variations, chromothripsis, driver mutations, apolipoprotein B mRNA-editing enzyme, catalytic polypeptide (APOBEC) mutational activity, and a progressive decrease in immunoglobulin transcription that inversely correlates with proliferation. Moreover, we identify frequent insertional mutagenesis by endogenous retro-elements as a murine specific mechanism to activate NF-kB and IL6 signaling pathways shared with human MM. Despite the increased genomic complexity associated with progression, advanced tumors remain dependent on
MYC
. In summary, here we credential the Vk*MYC mouse as a unique resource to explore MM genomic evolution and describe a fully annotated collection of diverse and immortalized murine MM tumors.
Mouse models often combine mutant alleles to accelerate cancer development, limiting oncogenic diversity. Here the authors show that sporadic MYC activation in Vk*MYC mice is sufficient to induce tumors with a variety of secondary mutations that mirror the genetic heterogeneity of human myeloma.
Publisher
Nature Publishing Group UK,Nature Publishing Group,Nature Portfolio
Subject
/ 38/23
/ 38/39
/ 38/90
/ 45
/ 64
/ 64/60
/ Animals
/ Cell Transformation, Neoplastic - genetics
/ DNA Copy Number Variations - genetics
/ Genomics
/ Humanities and Social Sciences
/ Humans
/ Mice
/ Multiple Myeloma - pathology
/ Mutation
/ Proto-Oncogene Proteins c-myc - genetics
/ Proto-Oncogene Proteins c-myc - metabolism
/ Science
/ Signal Transduction - genetics
/ Tumors
