{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,19]],"date-time":"2026-05-19T17:11:51Z","timestamp":1779210711577,"version":"3.51.4"},"reference-count":14,"publisher":"Oxford University Press (OUP)","issue":"5","license":[{"start":{"date-parts":[[2026,5,1]],"date-time":"2026-05-01T00:00:00Z","timestamp":1777593600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2026,5,5]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Objectives<\/jats:title>\n                    <jats:p>To characterize the genetic profiles of chronic myelomonocytic leukemia (CMML) cases that do not exhibit increased classical monocyte (CM) subsets in \u00adperipheral blood.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>A total of 174 patients with CMML who were treatment\u2011naive for hypomethylating agents and had undergone next\u2011generation sequencing (NGS) testing were analyzed. Among these, 152 patients (87.4%) demonstrated increased CM subsets (&amp;gt;94%) by flow cytometry (CM group), while 22 patients (12.6%) did not show increased CM subsets (\u226494%) (non\u2011CM group).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Patients in the CM and non\u2011CM groups exhibited comparable demographic characteristics, complete blood count parameters, CMML subtype (myelodysplastic vs myeloproliferative), and disease grade (CMML\u20111 vs CMML\u20112). The NGS analysis revealed significant enrichment of CBL (45.5% vs 11.2%, P\u2009&amp;lt;\u2009.001), IDH2 (18.2% vs 4.6%, P\u2009=\u2009.035), RAS pathway gene mutations (59.1% vs 34.2%, P\u2009=\u2009.033), and a lower frequency of TET2 mutations (40.9% vs 67.1%, P\u2009=\u2009.031) in the non\u2011CM group compared with the CM group. Patients with CMML in the non\u2011CM group also exhibited fewer cytogenetic abnormalities compared with those in the CM group (0% vs 22.5%, P\u2009=\u2009.039). Both non-CM and CBL-mutated CMML showed higher expression of HLA-DR by flow cytometry. No statistically significant differences were observed between the 2 groups in overall survival or acute myeloid leukemia\u2013free survival.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Chronic myelomonocytic leukemia without increased CM subsets is associated with a distinct genetic profile characterized by enrichment of CBL mutations. Mechanistically, we hypothesize that CBL mutations promote proinflammatory signaling that contributes to normalization of CM partitioning.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1093\/ajcp\/aqag045","type":"journal-article","created":{"date-parts":[[2026,4,9]],"date-time":"2026-04-09T11:48:41Z","timestamp":1775735321000},"source":"Crossref","is-referenced-by-count":0,"title":["Chronic myelomonocytic leukemia without increased classical monocyte subsets exhibits a distinct genetic profile, including frequent\n                    <i>CBL<\/i>\n                    mutations"],"prefix":"10.1093","volume":"165","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-2054-5986","authenticated-orcid":false,"given":"Mingfei","family":"Yan","sequence":"first","affiliation":[{"name":"Department of Pathology and Laboratory Medicine, H. Lee Moffitt Cancer Center & Research Institute , Tampa, FL,","place":["United States"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ismail Elbaz","family":"Younes","sequence":"additional","affiliation":[{"name":"Department of Pathology and Laboratory Medicine, H. Lee Moffitt Cancer Center & Research Institute , Tampa, FL,","place":["United States"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jinming","family":"Song","sequence":"additional","affiliation":[{"name":"Department of Pathology and Laboratory Medicine, H. Lee Moffitt Cancer Center & Research Institute , Tampa, FL,","place":["United States"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ling","family":"Zhang","sequence":"additional","affiliation":[{"name":"Department of Pathology and Laboratory Medicine, H. Lee Moffitt Cancer Center & Research Institute , Tampa, FL,","place":["United States"]}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"286","published-online":{"date-parts":[[2026,5,19]]},"reference":[{"key":"2026051912532838100_aqag045-B1","doi-asserted-by":"crossref","first-page":"e584","DOI":"10.1038\/bcj.2017.66","article-title":"Flow cytometry based monocyte subset analysis accurately distinguishes chronic myelomonocytic leukemia from myeloproliferative neoplasms with associated monocytosis","volume":"7","author":"Patnaik","year":"2017","journal-title":"Blood Cancer J"},{"key":"2026051912532838100_aqag045-B2","doi-asserted-by":"crossref","first-page":"3618","DOI":"10.1182\/blood-2015-01-620781","article-title":"Characteristic repartition of monocyte subsets as a diagnostic signature of chronic myelomonocytic 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glucocorticoid-treated patients with chronic myelomonocytic leukemia","volume":"108","author":"Watanabe","year":"2018","journal-title":"Int J Hematol"},{"key":"2026051912532838100_aqag045-B9","doi-asserted-by":"crossref","first-page":"e0183594","DOI":"10.1371\/journal.pone.0183594","article-title":"The MHC class II antigen presentation pathway in human monocytes differs by subset and is regulated by cytokines","volume":"12","author":"Lee","year":"2017","journal-title":"PLoS One"},{"key":"2026051912532838100_aqag045-B10","doi-asserted-by":"crossref","first-page":"581","DOI":"10.1111\/bjh.19060","article-title":"Phenotypic subtypes of leukaemic transformation in chronic myelomonocytic leukaemia","volume":"203","author":"Montalban-Bravo","year":"2023","journal-title":"Br J Haematol"},{"key":"2026051912532838100_aqag045-B11","doi-asserted-by":"crossref","first-page":"2883","DOI":"10.1038\/s41375-022-01727-6","article-title":"Srsf2(P95H\/+) co-operates with loss of TET2 to promote myeloid 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