{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,2]],"date-time":"2026-10-02T14:04:57Z","timestamp":1790949897732,"version":"4.1.0"},"reference-count":54,"publisher":"American Society of Hematology","issue":"21","content-domain":{"domain":["ashpublications.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2019,11,12]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>MYD88 L265P is the most common mutation in lymphoplasmacytic lymphoma\/Waldenstr\u00f6m 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 clonal, high-grade DLBCL. Murine findings regarding differences in the pattern of MYD88 staining and immune infiltrates in the bone marrows of MYD88 wild-type (MYD88WT) and MYD88L265P mice are recapitulated in the human setting, which provides insight into LPL\/WM pathogenesis. Furthermore, histologic transformation to DLBCL is associated with acquisition of secondary genetic lesions frequently seen in de novo human DLBCL as well as LPL\/WM-transformed cases. These findings indicate that, although the MYD88L265P mutation might be indispensable for the LPL\/WM phenotype, it is insufficient by itself to drive malignant transformation in B cells and relies on other, potentially targetable cooperating genetic events for full development of lymphoma.<\/jats:p>","DOI":"10.1182\/bloodadvances.2019000588","type":"journal-article","created":{"date-parts":[[2019,11,5]],"date-time":"2019-11-05T11:53:34Z","timestamp":1572954814000},"page":"3360-3374","update-policy":"https:\/\/doi.org\/10.1182\/blood.2019cm0000","source":"Crossref","is-referenced-by-count":29,"title":["Human MYD88L265P is insufficient by itself to drive neoplastic transformation in mature mouse B cells"],"prefix":"10.1182","volume":"3","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-4603-8517","authenticated-orcid":false,"given":"Tomasz","family":"Sewastianik","sequence":"first","affiliation":[{"name":"Department of Oncologic Pathology, Dana-Farber Cancer Institute, Harvard Medical 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