{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,28]],"date-time":"2026-08-28T15:25:43Z","timestamp":1787930743223,"version":"build-2784847793"},"reference-count":26,"publisher":"Walter de Gruyter GmbH","issue":"1","license":[{"start":{"date-parts":[[2026,1,1]],"date-time":"2026-01-01T00:00:00Z","timestamp":1767225600000},"content-version":"unspecified","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2026,1,23]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>BCR-ABL1 e6a2-positive chronic myeloid leukemia (CML) is a rare molecular subtype of CML, accounting for less than 1\u202f% of CML cases. It was shown to be associated with aggressive clinical behavior and a tendency toward disease progression. Here, we report a 56-year-old man who presented with pancytopenia, cervical lymphadenopathy, and severe myelofibrosis, without the typical leukocytosis observed in classic CML. Concurrent active pulmonary tuberculosis further complicated the diagnostic process. Hyperuricemia and elevated levels of lactate dehydrogenase (LDH) suggested a high cell-turnover state, and cervical lymph node biopsy confirmed myeloid sarcoma. Cytogenetic analysis revealed t(9;22)(q34;q11.2) with trisomy 8. Real-time quantitative polymerase chain reaction (RT-qPCR) identified the rare BCR-ABL1 e6a2 transcript. The patient received second- and third-generation tyrosine kinase inhibitor (TKI)-based therapy combined with chemotherapy. An individualized rifamycin-sparing anti-tuberculosis regimen was also prescribed. The patient achieved complete remission with marked regression of myelofibrosis. This case suggests that e6a2-positive CML may present with atypical features, including pancytopenia, severe myelofibrosis, and extramedullary blast crisis. In patients with concurrent tuberculosis, timely tissue biopsy and molecular testing are essential to accelerate diagnosis.<\/jats:p>","DOI":"10.1515\/biol-2025-1369","type":"journal-article","created":{"date-parts":[[2026,8,28]],"date-time":"2026-08-28T14:56:30Z","timestamp":1787928990000},"source":"Crossref","is-referenced-by-count":0,"title":["Myeloid sarcoma as EM blast crisis in BCR-ABL1 e6a2+ CML with myelofibrosis and TB: a case report"],"prefix":"10.1515","volume":"21","author":[{"given":"Chunling","family":"Gu","sequence":"first","affiliation":[{"name":"Graduate School , Hebei North University , Zhangjiakou , Hebei Province , 075000 , China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rui","family":"Lu","sequence":"additional","affiliation":[{"name":"Graduate School , Hebei North University , Zhangjiakou , Hebei Province , 075000 , China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yixin","family":"Kang","sequence":"additional","affiliation":[{"name":"The Eighth Medical Center, Chinese PLA General Hospital , Beijing , 100089 , China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wen","family":"Chen","sequence":"additional","affiliation":[{"name":"Department of Pathology , The Eighth Medical Center, Chinese People\u2019s Liberation Army (PLA) General Hospital , Beijing , China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yongqing","family":"Zhang","sequence":"additional","affiliation":[{"name":"Department of Hematology , The Eighth Medical Center of Chinese PLA General Hospital , Beijing , China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sainan","family":"Yang","sequence":"additional","affiliation":[{"name":"Department of Hematology , The Eighth Medical Center of Chinese PLA General Hospital , Beijing , China"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"374","published-online":{"date-parts":[[2026,8,31]]},"reference":[{"key":"2026082814562234162_j_biol-2025-1369_ref_001","doi-asserted-by":"crossref","unstructured":"Shammas, T, Peiris, MN, Meyer, AN, Donoghue, DJ. BCR-ABL: the molecular mastermind behind chronic myeloid leukemia. Cytokine Growth Factor Rev 2025;83:45\u201358. https:\/\/doi.org\/10.1016\/j.cytogfr.2025.05.001.","DOI":"10.1016\/j.cytogfr.2025.05.001"},{"key":"2026082814562234162_j_biol-2025-1369_ref_002","doi-asserted-by":"crossref","unstructured":"Cruz-Rodriguez, N, Tang, H, Rouhimoghadam, M, Liao, J, Bateman, B, Bates, B, et al.. Targeting chronic myeloid leukemia with potent and specific BCR::ABL1 degraders. Blood 2024;144:4157\u20138. https:\/\/doi.org\/10.1182\/blood-2024-211207.","DOI":"10.1182\/blood-2024-211207"},{"key":"2026082814562234162_j_biol-2025-1369_ref_003","doi-asserted-by":"crossref","unstructured":"Lucini, C, Sponseiler, I, Senkiv, J, Bandian, AM, Lion, T. Differential in vitro sensitivity of BCR::ABL1 kinase domain mutations to tyrosine kinase inhibitors depending on the p190 or p210 background. Blood 2024;144:2829. https:\/\/doi.org\/10.1182\/blood-2024-200428.","DOI":"10.1182\/blood-2024-200428"},{"key":"2026082814562234162_j_biol-2025-1369_ref_004","doi-asserted-by":"crossref","unstructured":"Hovorkova, L, Winkowska, L, Skorepova, J, Krumbholz, M, Benesova, A, Polivkova, V, et al.. Distinct pattern of genomic breakpoints in CML and BCR::ABL1-positive ALL: analysis of 971 patients. Mol Cancer 2024;23:138. https:\/\/doi.org\/10.1186\/s12943-024-02053-4.","DOI":"10.1186\/s12943-024-02053-4"},{"key":"2026082814562234162_j_biol-2025-1369_ref_005","doi-asserted-by":"crossref","unstructured":"Ramdohr, F, Fabarius, A, Maier, B, Bretschneider, D, Jauch, A, Monecke, A, et al.. Atypical presentation of patients with chronic myeloid leukemia in chronic phase\u2013Case report. 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