{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Sewastianik T"],"funding":["NCI NIH HHS"],"pagination":["3360-3374"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC6855113"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["3(21)"],"pubmed_abstract":["MYD88 L265P is the most common mutation in lymphoplasmacytic lymphoma/Waldenström macroglobulinemia (LPL/WM) and one of the most frequent in poor-prognosis subtypes of diffuse large B-cell lymphoma (DLBCL). Although inhibition of the mutated MYD88 pathway has an adverse impact on LPL/WM and DLBCL cell survival, its role in lymphoma initiation remains to be clarified. We show that in mice, human MYD88L265P promotes development of a non-clonal, low-grade B-cell lymphoproliferative disorder with several clinicopathologic features that resemble human LPL/WM, including expansion of lymphoplasmacytoid cells, increased serum immunoglobulin M (IgM) concentration, rouleaux formation, increased number of mast cells in the bone marrow, and proinflammatory signaling that progresses sporadically to clo"],"journal":["Blood advances"],"pubmed_title":["Human MYD88L265P is insufficient by itself to drive neoplastic transformation in mature mouse B cells."],"pmcid":["PMC6855113"],"funding_grant_id":["R01 CA196783"],"pubmed_authors":["Sewastianik T","Yang G","Jarolim P","Kofides A","Patel NA","Wright K","Treon SP","Jiang M","Shanmugam V","Nag A","Tanton H","Hunter ZR","Guerrera ML","Huang Y","Munshi NC","Adler K","Dalgarno A","Dennis PS","Carrasco RD","Demos MG","Pinkus GS"],"additional_accession":[]},"is_claimable":false,"name":"Human MYD88L265P is insufficient by itself to drive neoplastic transformation in mature mouse B cells.","description":"MYD88 L265P is the most common mutation in lymphoplasmacytic lymphoma/Waldenström macroglobulinemia (LPL/WM) and one of the most frequent in poor-prognosis subtypes of diffuse large B-cell lymphoma (DLBCL). Although inhibition of the mutated MYD88 pathway has an adverse impact on LPL/WM and DLBCL cell survival, its role in lymphoma initiation remains to be clarified. We show that in mice, human MYD88L265P promotes development of a non-clonal, low-grade B-cell lymphoproliferative disorder with several clinicopathologic features that resemble human LPL/WM, including expansion of lymphoplasmacytoid cells, increased serum immunoglobulin M (IgM) concentration, rouleaux formation, increased number of mast cells in the bone marrow, and proinflammatory signaling that progresses sporadically to clo","dates":{"release":"2019-01-01T00:00:00Z","publication":"2019 Nov","modification":"2026-05-04T11:20:37.094Z","creation":"2021-02-19T23:44:30Z"},"accession":"S-EPMC6855113","cross_references":{"pubmed":["31698464"],"doi":["10.1182/bloodadvances.2019000588"]}}