{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,15]],"date-time":"2026-07-15T05:05:45Z","timestamp":1784091945096,"version":"3.55.0"},"reference-count":39,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,7,15]],"date-time":"2026-07-15T00:00:00Z","timestamp":1784073600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/100000738","name":"U.S. Department of Veterans Affairs","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100000738","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Oncol."],"abstract":"<jats:sec>\n                    <jats:title>Introduction<\/jats:title>\n                    <jats:p>\n                      Natural Killer Lytic-Associated Molecule (NKLAM) (also known as RNF19b) is a membrane-bound E3 ubiquitin ligase. Previous studies demonstrated a role of NKLAM in natural killer (NK) cell function and pro-inflammatory cytokine production by macrophages. Studies using lymphoma, melanoma and breast cancer cells found that tumor dissemination and metastasis are greater in NKLAM-deficient knockout (KO) mice than in wild type (WT) mice, indicating that NKLAM participates in controlling tumor development\n                      <jats:italic>in vivo<\/jats:italic>\n                      .\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>We employed the E\u03bc-myc mouse model to determine whether NKLAM influences B cell lymphomagenesis. In young E\u03bc-myc mice, overexpression of myc in B lineage cells leads to expansion of non-neoplastic precursor B cells, which subsequently disappear. Over time, pre-B, pro-B or immature B cell lymphomas develop.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>NKLAM KO E\u03bc-myc mice have higher levels of precursor B cells than WT transgenic mice. These cells express more myc and Bcl-2 and persist longer. Lymphomas develop more rapidly in NKLAM KO E\u03bc-myc mice and strikingly, have a more differentiated phenotype, characterized by surface IgM. These lymphomas are also less aggressive than IgM- tumors when injected into non-transgenic mice. Infusion of NKLAM+ immune cells into young NKLAM KO E\u03bc-myc mice extends their survival, which increases the proportion of mice that develop more aggressive, immune-resistant IgM- lymphomas.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Discussion<\/jats:title>\n                    <jats:p>These studies indicate that NKLAM contributes to both the early and late phases of myc-driven B cell lymphomagenesis, first by limiting expression of myc and Bcl-2 within the non-malignant pre-B cells, resulting in longer tumor-free survival. This is followed by immunoediting by NKLAM+ immune cells, leading to development of IgM- lymphomas that are less immunogenic and more aggressive.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.3389\/fonc.2026.1874366","type":"journal-article","created":{"date-parts":[[2026,7,15]],"date-time":"2026-07-15T04:21:53Z","timestamp":1784089313000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["E3 ubiquitin ligase NKLAM\/RNF19b suppresses myc-driven B cell lymphomagenesis in E\u03bc-myc mice"],"prefix":"10.3389","volume":"16","author":[{"given":"Richard G.","family":"Hoover","sequence":"first","affiliation":[{"name":"Department of Pathology, Saint Louis University School of Medicine","place":["St. Louis, MO, United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Emily C.","family":"Matchett","sequence":"additional","affiliation":[{"name":"Department of Pathology, Saint Louis University 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