{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Maura F"],"funding":["U.S. Department of Health & Human Services | NIH | National Cancer Institute","NCI NIH HHS"],"pagination":["3844"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11076575"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["15(1)"],"pubmed_abstract":["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 pathway"],"journal":["Nature communications"],"pubmed_title":["The genomic landscape of Vk*MYC myeloma highlights shared pathways of transformation between mice and humans."],"pmcid":["PMC11076575"],"funding_grant_id":["R01 CA234181","CA186781","U01 CA271410","U54 CA224018","P30 CA240139","RO1CA234181","P50 CA186781","U54CA224018","R01 CA272426"],"pubmed_authors":["Du MT","Ziccheddu B","Landgren O","Tafoya Alvarado Y","Shi CX","Morgan GJ","Stein CK","Sharik ME","Braggio E","Zhu YX","Meermeier EW","Maura F","Chesi M","Coffey DG","Bergsagel PL"],"additional_accession":[]},"is_claimable":false,"name":"The genomic landscape of Vk*MYC myeloma highlights shared pathways of transformation between mice and humans.","description":"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 pathway","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 May","modification":"2026-06-03T04:22:49.98Z","creation":"2026-04-24T03:10:02.059Z"},"accession":"S-EPMC11076575","cross_references":{"pubmed":["38714690"],"doi":["10.1038/s41467-024-48091-w"]}}