---
title: "Distinguishing CML in Megakaryocytic Blast Crisis vs De Novo Ph+ Acute Megakaryoblastic Leukemia —"
id: "frontiers-in-immunology-12-distinguishing-chronic-myeloid-leukemia-in-megakaryocytic-blast-crisis-from-de"
canonical_url: "https://medichelpline.com/clinical-feed/frontiers-in-immunology-12-distinguishing-chronic-myeloid-leukemia-in-megakaryocytic-blast-crisis-from-de"
content_type: "clinical_feed_article"
specialty: "Oncology"
source_name: "Frontiers in Immunology"
source_url: "https://www.frontiersin.org/articles/10.3389/fimmu.2026.1812840"
published_at: "2026-07-29T00:00:00.000Z"
evidence_level: "Journal Feed"
license: "CC-BY-NC-4.0 / Informational Use"
---
# Distinguishing CML in Megakaryocytic Blast Crisis vs De Novo Ph+ Acute Megakaryoblastic Leukemia —
## Provenance & Clinical Metadata
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- **Specialty:** [Oncology](https://medichelpline.com/clinical-feed/oncology.md)
- **Primary Source:** Frontiers in Immunology
- **Source URL:** [Original Journal Publication](https://www.frontiersin.org/articles/10.3389/fimmu.2026.1812840)
- **Published At:** 2026-07-29T00:00:00.000Z
- **Evidence Rating:** Journal Feed
## Executive GIST (TL;DR)
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## Clinical Analysis & Structured Key Points
Frontiers | Distinguishing chronic myeloid leukemia in megakaryocytic blast crisis from de novo Ph+ acute megakaryoblastic leukemia: a case report and systematic review CASE REPORT article Front. Immunol. , 29 July 2026 Sec. Alloimmunity and Transplantation Volume 17 - 2026 | https://doi.org/10.3389/fimmu.2026.1812840 Published in Frontiers in Immunology Alloimmunity and Transplantation 7 impact factor 11.3 citescore Editor & Reviewers Edited by G C Gerhard C Hildebrandt Reviewed by T U Taha Ulutan Kars A A Abdul Ali Peer-Zada Outline Figures and Tables Figure 1 View in article Figure 2 View in article Figure 3 View in article Figure 4 View in article Figure 5 View in article Figure 6 View in article Figure 7 View in article Table 1 Summary of CML with MKBC as the initial manifest and de novo Ph+ AMKL cases. View in article Table 2 Major points of differentiation between CML-MKBC and Ph+ AMKL. View in article CASE REPORT article Front. Immunol. , 29 July 2026 Sec. Alloimmunity and Transplantation Volume 17 - 2026 | https://doi.org/10.3389/fimmu.2026.1812840 Distinguishing chronic myeloid leukemia in megakaryocytic blast crisis from de novo Ph+ acute megakaryoblastic leukemia: a case report and systematic review Q L Qingqing Liu 1 P Y Pu Yu 1 X L Xiaozhen Li 2 H L Hai Lan 2,3 Z L Zenghui Liu 2 * 1. The First Clinical Medical School of Guangzhou University of Chinese Medicine, Guangzhou, China 2. Department of Hematology, the First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, China 3. Department of Hematology, the Shunde Hospital of Guangzhou University of Chinese Medicine, Guangzhou, China See more Article metrics View details Abstract Chronic myeloid leukemia (CML) with megakaryoblastic blast crisis (MKBC) as the initial manifestation is extremely rare, accounting for less than 3% of all CML cases. Philadelphia chromosome-positive acute myeloid leukemia, FAB M7 subtype (Ph+ AML-M7), is also known as Philadelphia chromosome-positive acute megakaryoblastic leukemia (Ph+ AMKL), representing a distinct and prognostically unfavorable category of AML. Morphologically and immunophenotypically, these two entities are nearly identical, posing significant diagnostic challenges. We describe a novel case of Ph+ leukemia with MKBC differentiation that appears most consistent with CML in blast phase (BP). Following treatment with a tyrosine kinase inhibitor (TKI) combined with induction and consolidation chemotherapy, the patient achieved complete remission (CR). Although hematopoietic stem cell transplantation (HSCT) was declined due to economic constraints, the patient has maintained deep molecular remission(MR5, BCR::ABL1 IS ≤ 0.001%)for 35 months to date. Through a systematic review of existing literature, this article elucidates key discriminative features between the two conditions and proposes a practical diagnostic and therapeutic framework to guide clinical decision-making. Introduction Chronic myeloid leukemia (CML) is a myeloproliferative neoplasm driven by the BCR::ABL1 fusion gene, typically progressing from chronic phase (CP) through accelerated phase (AP) to blast phase (BP) if untreated ( 1 , 2 ). BP is defined by the presence of ≥20% blasts in peripheral blood or bone marrow (BM) and is associated with poor prognosis. Among various differentiation lineages, megakaryoblastic blast crisis (MKBC) is exceedingly rare, accounting for less than 3% of all CML transformations, and cases presenting with MKBC as the initial manifestation are even rarer ( 3 ). Philadelphia chromosome-positive acute megakaryoblastic leukemia (Ph+ AMKL) is a distinct entity that also presents with megakaryoblastic differentiation and carries the t (9;22) translocation but lacks a prior CP history of CML. Distinguishing CML-MKBC from de novo Ph+ AMKL is clinically challenging yet critical, as treatment strategies differ substantially. Herein, we report a rare case of Ph+ leukemia with MKBC differentiation that appears most consistent with CML-BP. We systematically review the literature, compare clinical, immunophenotypic, and molecular features between these two entities, and propose a practical diagnostic and therapeutic framework to assist clinicians in this challenging differential diagnosis. Case presentation A 49-year-old male presented to the Department of Hematology, first Affiliated Hospital of Guangzhou University of Chinese Medicine, in February 13, 2023, reporting a one-month history of upper abdominal distension and pain. The patient had no record of hematological abnormalities before admission, and there were no antecedent features of CML-CP (e.g., fatigue or night sweats) reported by the patient. Laboratory investigations revealed leukocytosis (white blood cell count 58.63×10⁹/L) and anemia (hemoglobin 74 g/L). Abdominal ultrasound demonstrated marked splenomegaly. Peripheral blood smear revealed 22% blasts with megakaryocytic features and 8% basophils. BM aspirate smears showed marked megakaryocyte proliferation with dysplasia. Megakaryoblasts accounted for 52% of nucleated cells, basophils were markedly increased, constituting 10.5% of nucleated cells ( Figure 1A ). BM biopsy demonstrated grade III myelofibrosis, CD61+ atypical cells, and markedly reduced granulocytic (MPO+) and erythroid (CD71+) series by immunohistochemistry ( Figure 1B ). Flow cytometry immunophenotyping of the blast population revealed co-expression of megakaryocytic markers (CD41, CD61) and progenitor markers (CD34, CD117) with aberrant myeloid-associated markers (CD13, CD33). Myeloperoxidase (MPO) was negative, and B-cell markers were absent, effectively excluding alternative lineages ( Figure 2 ). Immunohistochemistry confirmed the megakaryoblastic lineage of the infiltrating cells through CD61 staining at the tissue level and demonstrated severe suppression of normal granulocytic and erythroid hematopoiesis. Cytogenetic analysis showing a complex karyotype, including a hyper-tetraploid, double-Ph clone and translocation between 9q34 and 22q11.2, and no other cytogenetic abnormalities were found ( Figure 3 ). BCR-ABL fusion gene screening was performed on BM aspirate using a multiplex real-time quantitative PCR panel for 56 leukemia-associated fusion genes. Diagnostic quantitative PCR detected BCR::ABL1(p210) transcript with a BCR::ABL1 IS of 144.21%. Next generation sequencing was performed using the hematopoietic and lymphoid neoplasms gene mutation panel (222 genes): ASXL1 NM_015338.6:c.1860_1861delTG (p.Ala621fs) (30.60%), ASXL1 NM_015338.6:c.1934dupG (p.Gly646fs) (12.64%), CSF1R NM_005211.3:c.2056_2079del (p.Ser686_Pro693del) (42.80%), PTPN11 NM_002827.4:c.167G>A (p.Arg56Gln) (8.70%), and RELN NM_005045.4:c.10108A>G (p.Thr3370Ala) (49.30%), and no other gene mutations were detected. Figure 1 (A) Bone marrow aspirate smear (Wright-Giemsa stain, ×1000) showing leukemic blast cells and megakaryocytes. These blasts exhibited rounc nuclei with fine chromatin and basophilic cytoplasm, some showing cytoplasmic blebbing. (B) Bone marrow biopsy (HE stain, ×200) showing diffuse fibrous tissue hyperplasia and scattered atypical nucleated cells; inset: reticulin stain (+) indicating grade III fibrosis. Figure 2 Flow cytometry was performed on bone marrow aspirate using a CD45/SSC gating strategy, a distinct blast population (Population A) was identified in the CD45-dim/SSC-low region, accounting for 46.3% of total nucleated cells, immunophenotyping analysis of the blast gate showed negativity for CD56, CD20, and CD79a, and positivity for HLA-DR, CD34, CD117, CD13, CD33, CD41, CD61, and CD38. Figure 3 Chromosome karyotype 46, XY, t (9; 22) (q34; q11.2) [15]/92, XXYY, t (9; 22) (q34; q11.2) x 2 [2]. 46, XY, t(9;22)(q34;q11.2) in 15 of 17 metaphases, the remaining two metaphases showed a tetraploid karyotype 92, XXYY, t(9;22)×2, and translocation between 9q34 and 22q11.2. Although the patient’s BM morphology, flow cytometry immunophenotyping, absence of prior CML history, and BCR::ABL1(p210) positivity closely aligned with diagnostic criteria for Ph⁺ AMKL, the presence of splenomegaly and significant basophilia at presentation strongly supported a diagnosis of CML presenting with megakaryocytic blast crisis (MKBC) as the initial manifestation. Targeted fluorescence in situ hybridization (FISH) to determine whether BCR::ABL1 signals are present across differentiated myeloid lineages—considered a gold standard for distinguishing CML-BP from de novo Ph+ AMKL—was not available in our laboratory. Therefore, the diagnosis relies on a composite of clinical, morphologic, karyotype, and molecular features. Therapy and prognosis The patient initially received induction chemotherapy with the MA regimen, consisting of mitoxantrone 10 mg/m² on days 1–3, combined with cytarabine 100 mg every 12 hours on days 1–7. Additionally, the tyrosine kinase inhibitor (TKI) imatinib was concurrently administered orally at a dose of 400 mg twice daily. One month later, the BM morphology confirmed complete remission (CR), and BCR::ABL1 IS (p210) levels declined from 144.21% to 1.07%. He subsequently received alternating cycles of induction and consolidation therapy, with regular monitoring of BCR::ABL1 IS (p210) ( Figure 4 ). Between May and June 2023, consolidation therapy consisted of cytarabine (3.5 g IV every 12 h on days 1, 3, and 5) along with imatinib (600 mg once daily). Repeat BM examination demonstrated sustained CR, with BCR::ABL1 IS (p210) further decreasing to 0.07%, achieving a major molecular response (MMR). Figure 4 BCR::ABL1 IS values over treatment time. Given the high-risk profile conferred by adverse genetic abnormalities and the patient’s sustained CR status, hematopoietic stem cell transplantation (HSCT) was recommended. However, the patient declined due to financial constraints. Subsequently, from July to December` 2023, he received alternating cycles of the MA regimen and cytarabine-based regimens. Although hematologic remission persisted, subsequent monitoring revealed molecular relapse with BCR::ABL1 IS (p210) rising to 0.18% and 0.62% over the following two months; therefore, from April to November 2024, the patient received two courses of the HA regimen (homoharringtonine 3.6 mg IV on days 2–6 plus azacitidine 100 mg subcutaneously on days 1–7) and one additional course of the MA regimen, while continuing imatinib (600 mg once daily). During treatment, the patient developed grade IV myelosuppression complicated by Klebsiella pneumoniae septicemia, which resolved with anti-infective therapy and supportive measures (e.g., antibiotics and platelet transfusions). Flow cytometry in November 2024 showed undetectable blasts, and by May 2025, BCR::ABL1 IS (p210) was undetectable. To date, the patient has maintained deep MR5 for 35 months according to the 2025 ELN recommendations for the management of CML ( 4 ). Discussion Diagnosis and differential Ph+ AML was originally recognized as CML-BP but was recognized as a distinct entity in the 2016 WHO classification of Myeloid Neoplasms and Acute Leukemia ( 5 ), and there is no unified standard to distinguish CML-MKBC from Ph+ AMKL at present. In order to summarize the main distinguishing points of the two entities, a systematic literature search was conducted following PRISMA guidelines in PubMed/MEDLINE, Web of Science, Scopus, and Google Scholar from inception to February 2026 ( Figure 5 ). A total of 195 records were identified, and ultimately 11 cases of CML with MBKC as the first episode ( 3 , 6 – 15 ) and 9 cases of Ph+ AMKL have been reported ( 16 – 23 ). Data in the currently summarized literature are partially incomplete, we have collected recorded information ( Table 1 ). Figure 5 Decision tree for WHO/ICC classification of suspected CML with megakaryocytic crisis. A. 11 cases of CML with MKBC as the initial manifest. Authors Year Peripheral Splenomegaly BM Characteristics Treatment Survival (moa a ) WBCs (x10^9/L) Basophils (%) Blasts (%) Immunophenotype Cytogenetics BCR /ABL Fibrosis CD Wu et al. ( 6 ) 1996 19 2 No dry tap CD43, Factor VIII 46,XX,t(9;22)(q34.1;q11.2) NA ND b Ara-C c +etoposide with HSCT Died Hirose Yet al. ( 7 ) 2002 2.6 1 Yes 20 CD13,CD33,CD34,CD41a,HLA-DR NA 210 ND VP d +MTX e +6- MP f IME g 1 Pelloso F et al. ( 8 ) 2002 11.4 8 Yes 23 CD13, CD33, CD34, CD41, CD45, CD61, HLA-DR 46,XX,t(9;22)(q34.1;q11.2) 210 2 DA h with IM 6 Campiotti L et al. ( 9 ) 2007 9.9 7 Yes 56 CD13, CD33, CD34, CD41, CD45, CD61, HLA-DR 46,XX,t(9;22)(q34;q11) 210 ND IA i with IM 4 Bryant BJ et al. ( 10 ) 2007 23.8 11 Yes dry tap CD31, CD43, CD45 46,XX,t(9;22)(q34.1;q11.2) NA ND Hydroxyurea and radiation Died Pullarkat ST et al. ( 11 ) 2008 16.2 0 No dry tap CD7, CD33, CD41, CD45 64,XY with duplicate Ph chromosome NA ND IM Died Al-Shehri A et al. ( 12 ) 2010 36 4 Yes 50 CD41,CD42,CD61 46,XX,t(9;22)(q34;q11) 210 ND ITA j with IM+CBT k 22 Lu jin et al. ( 13 ) 2011 38.04 8 Yes 20 CD7, CD9, C13, CD33, CD34, CD38, CD41, CD61, CD117, CD123, HLA-DR 46XY,t(9;22)(q34;q11) 210 3~4 HA l DA with IM, Nilotinib NA Karkuzhali P et al. ( 14 ) 2013 27.9 4 Yes dry tap NA NA 210 2 ADE m with IM Died Sasaki H et al. ( 15 ) 2019 52.4 29 Yes 30 CD33, CD34, CD42b, Factor VIII, MPO NA 210 2 Dasatinib,Ponatini b,HSCT,CBT 12 Agrawa S et al. ( 3 ) 2020 1.34 NA Yes dry tap CD13, CD38, CD45, HLA-DR NA 210 3 DA with Dasatinib 2 B. 9 cases of de novo Ph+ AMKL. Authors Year Peripheral Splenomegaly BM Characteristics Treatment Survival (mos s ) WBCs (x10^9/L) Basophils (%) Blasts (%) Immunophenotype Cytogenetics BCR/ABL Fibrosis Cuneo A et al. ( 16 ) 1996 29 NA Yes 58 CD7,CD33,CD41,TdT 46,XX, t(9;22)(q34;q11), t(2;9)(q12;q33) NA ND NA 8 Mozziconacci MJ et al. ( 17 ) 1998 NA NA No NA NA 46,XX,inv(3)(q21q26)[4]/46,idem,t(9;22)(q3 4;q11)[15] NA NA NA Died Balatzenko G et al. ( 18 ) 2004 1.1 NA No 48 CD2,CD3,CD4,CD5,CD7,CD10,CD13,CD14,CD16,CD19,CD2 0,CD22,CD33,CD34,CD38,CD 56,CD61,CD62,HLA-DR 47,XX,+8,t(9; 22)(q34;q11) P190 ND NA Died Soupir CP et al. ( 19 ) 2007 23.2 0 Yes 93 ND 46,XY,t(9;22;21)(q34;q11;p11)[20] P210 ND NA 15 15.3 2 No 28 ND 46,XY,t(9;22)(q34;q11)[20] 46,XY,t(9;22)(q34;q11)[1]/46XY,t(5;11) (q13;21),t(9;22)(q34;q11)[4]/46XY,der(4),t(1;4)(q12;p16),t(5;11)(q13;q21),t(9;22)(q34; q11)[8]/46XY,der(4),t(1;4)(q12;p16),t(5;11) (q13;q21),del(6)(p21),t(9;22)(q34;q11),17,+ mar1[4] P210 ND NA 13 Papageorgiou SG et al. ( 20 ) 2010 22 NA Yes 50 CD34+,CD61+ P210 ND IDA-FLAG n +IA +Dasatinib 24 Han ying et al. ( 21 ) 2014 3.63 NA No 61.2 CD7,CD13,CD33,CD34,CD41, CD61,CD64,CD123,HLA-DR 46,XY,t(9;22)(q34;q11)[3]/46,XX[2] NA ND TA o +ME p +FL AG q +HP r +IM Died Min GJ et al. ( 22 ) 2018 NA NA No NA NA 46,XX,t(9;22)(q34;q11.2)[20] NA ND IA+IM Died Kashima E et al. ( 23 ) 2021 2.2 2 No NA CD13,CD34,CD117,HLA-DR 44,XX,der(3)(p21),add(4)(q21),add(5)(q22), del(15)(q11.2q15),-16add(17)(q25),-19 NA 2 IA 4 a, month; b, not detected; c, cytarabine; d, vincristine and prednisone; e, methotrexate; f, 6-mercaptopurine; g, Imatinib; h, daunorubicin and cytarabine; i, idarubicin and cytarabine; j, idarubicin, thioguanine and cytarabine; k, cord blood transplantation; l, homoharringtonine and azacitidine; m, adriamycin, cytarabine and etoposide; n, idarubicin, fludarabine and cytarabine; o, pirarubicin and cytarabine; p, mitoxantrone and etoposide; q, fludarabine and cytarabine; r, hydroxycamptothecin and etoposide. n, idarubicin; fludarabine and cytarabine; o, pirarubicin and cytarabine; p, mitoxantrone and etoposide; q, fludarabine and cytarabine; r, Hydroxycamptothecin and etoposide. Key distinguishing features between CML-MKBC and Ph+ AMKL emerged from this analysis. Splenomegaly was present in almost all reported CML-MKBC cases but is rare in de novo Ph+ AMKL. Basophilia (≥2% in peripheral blood or BM) was present in 80% of CML-MKBC cases, whereas it was observed in only isolated cases of Ph+ AMKL and never exceeded 2%. Regarding BCR::ABL1 transcript types, the p210 isoform was uniformly detected in CML-MKBC, whereas p190 was also observed in de novo Ph+ AMKL. Notably, leukocytosis with elevated white blood cell counts was a characteristic feature of CML-MKBC, whereas no consistent changes were observed in Ph+ AMKL. BM fibrosis (grade II-IV) was present in both entities but tended to be more severe in CML-MKBC. Karyotype analysis showed that CML-MKBC had clonal evolution such as double Ph, while Ph+ AMKL was accompanied by different complex abnormalities. Pullarkat et al. ( 11 ) used targeted FISH technology to confirm that BCR::ABL1 fusion signal existed not only in primordial megakaryocytes, but also in differentiated neutrophils, and the signal may be enhanced in primordial cells, which was the decisive evidence for the diagnosis of CML-BP. Conversely, if the signal is limited to blast cells, it is more likely to be primary Ph+ AMKL ( 19 ). Because BCR::ABL1 expression in CML-BP is “systemic” and present throughout the myeloid lineage; In contrast, De novo Ph+ AMKL expression is “focal” and restricted to the leukemic cells themselves. Therefore, determining the breadth of BCR::ABL1 clones is also the key to differentiate CML-MKBCs from Ph+ AMKL. When we encounter suspected Ph+ AMKL patients in clinical, in addition to BM and laboratory examination, we must also inquire whether there are features such as splenomegaly or basophilia. If conditions permit, it is recommended to use targeted FISH and other techniques to search for evidence of BCR::ABL1 in differentiated myeloid cells for differentiation from CML-MKBC. Unfortunately, targeted FISH testing was not performed in this case due to the unavailability of this technology in our laboratory, therefore, definitive proof of clonal origin of the megakaryoblasts from the Ph+ stem cell could not be established. However, the absence of a prior CP history and the presence of pan-myeloid dysplasia make the diagnosis of Ph+ AMKL less likely. Based on the existing records at present, we have summarized the key points for differentiating CML-MKBC and Ph+ AMKL, as detailed in Table 2 . Table 2 Items Favor to CML-MBC Favor to Ph+ AMKL Previous history Acute onset, no prior CML history Clinical feature Common splenomegaly and basophilia(>2%) Rare splenomegaly and basophilia BM blasts 20~60% 28~95% (often markedly higher) Immunophenotype CD41+/CD61/CD42 Cytogenetics 100% Ph chromosome positive, additional clonal chromosomal, such as double Ph del (3),der (4), del (6),del (15), +8, -19, +mar1, etc. BCR-ABL type P210 Predominantly P210, also P190 Fibrosis 2~4 Hardly ever Major points of differentiation between CML-MKBC and Ph+ AMKL. Distinguishing CML-MKBC from de novo Ph+ AMKL is challenging but clinically relevant. To address this diagnostic dilemma, we propose a stepwise diagnostic algorithm grounded in WHO 2022 ( 24 ) and ICC classifications ( 25 ) ( Figure 6 ). Applying this algorithm to our case, upon presentation, BM showed 52% megakaryoblasts and had no history of CML-CP. The presence of four features—BCR::ABL1(p210) transcript was positive, 10.5% basophilia in BM, grade III fibrosis, and splenomegaly further evidence that CML may present initially in MKBC. Some studies have found that +Ph is more common in different stages of CML ( 26 ). And the karyotype showed that 15 cells harbored the Ph chromosome as the first clone, the original first clone acquired new genetic abnormalities during disease progression and evolved into a more malignant subclone, that is, two cells found to be tetraploid (92, XXYY) and contain double-Ph, which is a typical “clonal evolution” ( 27 ). It is also one of the gold standards for the diagnosis of CML-BP ( 28 ). In addition, ASXL1 and PTPN11 detected in genes are the common mutation spectrum of CML-BP, thereby driving cell clonal hematopoiesis and leading to the occurrence of hematological tumors ( 29 – 31 ). The quantification of high BCR::ABL1(p210) expression in this patient indicated that there were a large number of leukemia clones with active pr
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