Acute myeloid leukemia with CBFB::MYH11 is one of the two canonical core-binding-factor (CBF) leukemias. It results most often from inv(16)(p13.1q22) and less commonly from t(16;16)(p13.1;q22). WHO-HAEM5 and the International Consensus Classification recognize this as an AML entity defined principally by the recurrent genetic abnormality rather than by strict reproduction of the historical French-American-British M4Eo phenotype [1, 2]. The rearrangement juxtaposes CBFB at 16q22 with MYH11 at 16p13.1 and generates the CBFβ-smooth muscle myosin heavy chain oncoprotein. The fusion disrupts normal RUNX1/CBFβ transcriptional regulation and creates a differentiation block; cooperating mutations, especially in signaling pathways, contribute to overt leukemogenesis and clonal evolution [14-18]. The marrow shows myelomonocytic differentiation and abnormal eosinophilic precursors containing coarse purple-violet or basophilic granules, often concentrated in the immature cytoplasm. These cells belong to the leukemic clone. Their abundance, however, is variable: genetically confirmed cases may have only a limited abnormal eosinophilic subset, monoblastic predominance, or atypical morphology associated with uncommon fusion transcripts [4-10]. Flow cytometry is useful for lineage assignment, recognition of phenotypic heterogeneity, and establishment of a baseline for measurable residual disease (MRD), but no immunophenotypic pattern is specific for inv(16). Conventional chromosome analysis documents clonal architecture, while CBFB break-apart FISH supplies rapid locus-specific evidence of rearrangement. Because a break-apart assay neither identifies MYH11 directly nor defines the fusion transcript, reverse-transcription polymerase chain reaction or RNA-based sequencing remains preferable when available, particularly for molecular MRD monitoring [10, 13, 19, 22]. We report an inv(16)-positive AML in which the abnormal eosinophilic precursor population was diagnostically informative but non-dominant within a blast-rich myelomonocytic marrow. The case illustrates the need to interpret differential counts hierarchically and to integrate morphology with orthogonal cytogenetic methods. Fig 1: Bone marrow aspirate smears stained with Leishman-Giemsa stain (×100 objective). (A) The red arrow indicates an immature abnormal eosinophilic precursor with coarse basophilic granules; the black arrow indicates a monocytoid blast/promonocyte. (B) The red arrow indicates an abnormal eosinophilic precursor with mixed granulation; black arrows indicate monoblasts/promonocytes with folded or indented nuclei and prominent nucleoli. Fig 2: Patient-specific conventional cytogenetic findings. (A) Representative GTG-banded metaphase with the abnormal chromosome 16 indicated by a red arrow. (B) Representative karyogram demonstrating inv(16)(p13.1q22); the abnormal chromosome 16 is marked by a red arrow. Fifteen of 20 metaphases carried the inversion. Reported ISCN: 46,XY,inv(16)(p13.1q22)[15]/46,XY[5]. Fig 3: Patient-specific CBFB break-apart FISH. The lower-left nucleus shows the normal 2F pattern. The upper-right nucleus shows one retained fusion signal with separated red and green signals (1F1R1G), consistent with CBFB rearrangement. The laboratory reported 160 of 200 abnormal nuclei (80%), above the validated cutoff of 3%. Case report Clinical history and initial laboratory findings A 25-year-old man presented with excessive fatigue for approximately one month, intermittent fever for one month, and cough for two months. Examination showed severe pallor, hepatomegaly approximately 2 cm below the right costal margin, and splenomegaly approximately 2 cm below the left costal margin. During the preceding month, he had received three units of packed red blood cells and four units of random-donor platelets. The earliest available complete blood count showed hemoglobin 6.7 g/dL, total leukocyte count 72 × 10⁹/L, and platelet count 46 × 10⁹/L. An outside peripheral-blood differential classified approximately 20% atypical mononuclear cells and recommended urgent marrow evaluation. On the following day, hemoglobin was 5.1 g/dL, total leukocyte count 82 × 10⁹/L, and platelet count 25 × 10⁹/L. The patient was admitted with suspected acute leukemia. Platelet support was administered, bone marrow aspiration was performed, and hydroxyurea was prescribed briefly for cytoreduction. Detailed trephine-biopsy findings, definitive chemotherapy, treatment response, molecular MRD results, and longitudinal outcome were not available for review. Bone marrow morphology and differential count The aspirate contained hypercellular marrow particles and trails. Megakaryopoiesis and residual background granulopoiesis were markedly suppressed, while erythroid precursors were absent to negligible. A 500-cell differential count, calculated from all nucleated marrow cells, comprised 44% conventional blasts, 20% monoblasts/promonocytes, 6% monocytes, 12% eosinophils, 8% abnormal eosinophil precursors, and 10% lymphocytes. Because erythroid cells were absent to negligible, the all-nucleated-cell denominator effectively corresponded to the non-erythroid marrow-cell denominator; therefore, the eosinophilic-lineage percentages may be interpreted relative to non-erythroid marrow cells. Monoblasts and promonocytes are counted as blast equivalents in AML with monocytic or myelomonocytic differentiation; therefore, the blast-equivalent burden was 64%. Inclusion of the 6% more mature monocytes produced a combined 70% conventional-blast plus monocytic-lineage compartment [2, 3]. Blasts had high nuclear-to-cytoplasmic ratios. Monoblasts and promonocytes showed more abundant cytoplasm, folded or indented nuclei, and conspicuous nucleoli. Immature abnormal eosinophilic precursors contained strikingly coarse, deeply basophilic granules. A harlequin-type eosinophil, characterized by admixed eosinophilic and basophilic granules within the same cell, was also identified. Harlequin morphology is a useful clue but is not specific for inv(16) [4, 5, 30]. The available record noted myeloperoxidase positivity in immature myeloid cells, supporting myeloid lineage; however, the original cytochemical preparation and technical details were not available for independent review. Flow cytometry Flow cytometry had been performed at an outside laboratory before referral for cytogenetic testing. The available interpretive report described two abnormal compartments on CD45-versus-side-scatter analysis: (1) a primitive, low-side-scatter blast population expressing CD34, CD117, CD13, and CD33, with aberrant CD7 expression; and (2) a monoblastic/monocytic precursor population. This pattern was concordant with the separately enumerated conventional-blast and monocytic-lineage compartments. Aberrant CD7 represented a potential leukemia-associated immunophenotype, but antigen stability could not be assessed without follow-up samples [10, 11, 22]. Raw FCS files, original dot plots, the complete antibody panel, antigen-expression percentages and intensities, gating strategy, and specimen-quality metrics were unavailable for independent review. Consequently, flow cytometry was interpreted as supportive evidence of myeloid/monocytic differentiation and phenotypic heterogeneity. Conventional cytogenetics Conventional chromosome analysis was performed on bone marrow cells using a 24-hour unstimulated culture. Cells were cultured in RPMI-1640 medium supplemented with fetal calf serum, L-glutamine, penicillin, and streptomycin. Colcemid exposure, hypotonic treatment with 0.075 mol/L potassium chloride, methanol-acetic acid fixation, slide preparation, and GTG banding were performed according to the validated laboratory standard operating procedure and established cytogenetic methods [13, 34]. Twenty metaphases were analyzed at an approximate 300–400-band level using an Olympus BX-63 microscope and Applied Spectral Imaging software (version 8.3.2). Five representative metaphases were fully karyotyped. The result, reported according to ISCN 2024, was 46,XY,inv(16)(p13.1q22)[15]/46,XY[5]. No additional clonal chromosome abnormality was identified [13]. CBFB break-apart fluorescence in situ hybridization Interphase FISH was performed using a Wuhan HealthCare Biotechnology dual-color CBFB break-apart probe according to the manufacturer’s instructions. Two hundred interphase nuclei were evaluated. The laboratory-validated cutoff was 3%, and 160 of 200 nuclei (80%) showed an abnormal 1F1R1G pattern; the remaining 40 nuclei showed the normal 2F pattern. The ISCN result was nuc ish(CBFB)x2(5′CBFB sep 3′CBFB)x1[160/200] [12, 13]. The split-signal pattern demonstrated rearrangement of the CBFB locus and was concordant with cytogenetically visible inv(16). Because a break-apart assay does not identify the partner gene or define the fusion transcript, the integrated result was regarded as consistent with CBFB::MYH11-associated AML rather than direct molecular demonstration of the transcript [12, 19-22]. Integrated diagnosis Acute myeloid leukemia with inv(16)(p13.1q22) and CBFB rearrangement, consistent with CBFB::MYH11-associated core-binding-factor AML. The diagnosis was based on the convergence of a 64% blast-equivalent burden, monocytic differentiation, morphologically abnormal eosinophilic precursors, clonal inv(16) in 15 of 20 metaphases, and a conventional CBFB break-apart pattern in 80% of interphase nuclei. Under WHO-HAEM5 and ICC criteria, the recurrent genetic abnormality takes precedence over a generic differentiation-based AML category [1-3].

Incidence and diagnostic prevalence Population-based incidence and survivor prevalence specifically attributable to AML with inv(16)/CBFB::MYH11 are not well established. The abnormality is generally identified in approximately 4–8% of adult AML and about 8% of pediatric AML, although reported diagnostic frequencies vary according to age, referral population, and testing methodology. A four-center study detected inv(16)/t(16;16) in 27 of 412 AML cases (6.6%), while an Indian multiplex RT-PCR series identified CBFB::MYH11 in 2 of 96 adult cases (2.1%) and 2 of 20 pediatric cases (10%) [35-37]. This case emphasizes that the marrow differential should be interpreted as a biologic composition rather than as isolated percentages. Conventional blasts constituted 44%, while monoblasts/promonocytes contributed a further 20% blast equivalents, producing a total blast-equivalent burden of 64%. The additional 6% monocytes represented a more mature component of the same differentiation continuum but were not counted as blast equivalents [2, 3]. The eosinophilic-lineage compartment totaled 20%, of which 8% consisted of morphologically abnormal precursors. The present case represents a blast-rich myelomonocytic leukemia with a non-dominant abnormal eosinophilic subset. In inv(16)-associated AML, the diagnostic information supplied by eosinophils is primarily qualitative: coarse basophilic or purple-violet granules in immature eosinophilic cells are more informative than an isolated numerical increase in otherwise conventional eosinophils. Combined morphology-FISH studies have shown that these abnormal eosinophils are part of the leukemic clone [6]. Because erythroid precursors were absent to negligible and the 500-cell differential was calculated from all nucleated marrow cells, the denominator effectively corresponded to non-erythroid marrow cells. Historically, the FAB morphologic criteria for acute myelomonocytic leukemia required both granulocytic and monocytic components to constitute at least 20% of bone marrow non-erythroid cells, while the M4Eo variant was characterized by at least 5% marrow eosinophils, including abnormal immature forms with coarse purple-violet or basophilic granules [5, 38]. In our case, the monocytic component constituted 26% (20% monoblasts/promonocytes and 6% monocytes), and the eosinophilic-lineage component constituted 20% (12% eosinophils and 8% abnormal eosinophilic precursors), thereby exceeding the historical monocytic and eosinophilic thresholds. Nevertheless, the myelomonocytic morphology, characteristic abnormal eosinophils, and harlequin-type cells were strongly supportive, while inv(16) and CBFB rearrangement established the diagnosis under contemporary genetically defined classification [2, 3]. The harlequin-type eosinophil was visually striking but not pathognomonic. Similar hybrid granulation may occur in chronic myeloid leukemia and other myeloid disorders; therefore, it should prompt targeted genetic evaluation rather than serve as an independent diagnostic criterion [5, 30]. The morphologic spectrum of CBFB::MYH11 AML is broader than the historical M4Eo prototype. Cohorts and case reports document monoblastic predominance, limited abnormal eosinophils, atypical immunophenotypes, and uncommon fusion transcripts with non-classic morphology [7, 10, 31]. The reported two-compartment flow pattern was biologically coherent with the differential count: the CD34/CD117-positive primitive population corresponded to conventional blasts, while the second compartment paralleled monoblastic/monocytic differentiation. Nevertheless, CD34, CD117, CD13, CD33, aberrant CD7, and monocytic markers are not genotype-specific. Flow-cytometric MRD may be complementary to molecular MRD, but direct fusion-transcript quantification is the preferred disease-specific approach when a trackable CBFB::MYH11 transcript has been established [10, 11, 19, 22]. Orthogonal cytogenetic testing was decisive. The inversion was present in 15 of 20 metaphases, establishing a dominant clone, and the CBFB split signal was present in 80% of nuclei, far above the validated cutoff. Break-apart FISH is highly useful for rapid confirmation but may also produce atypical or discordant patterns; its result must therefore be interpreted with the karyotype, morphology, and, where possible, transcript testing [12, 13]. Secondary cytogenetic abnormalities are well documented in CBF-AML, although none was identified in this case [33]. CBFB::MYH11 AML is assigned to the ELN 2022 favorable-risk group, but relapse remains clinically important. Cooperating mutations in KIT, FLT3, RAS-pathway genes, and other pathways influence clonal behavior, although their prognostic effect depends on mutation type, burden, and interaction with MRD response. Recent studies support integrated assessment of baseline genetics and early molecular response rather than reliance on a single mutation [3, 14-18, 27, 32]. For medically fit adults, contemporary treatment generally uses intensive cytarabine-containing induction and cytarabine-intensive consolidation. Gemtuzumab ozogamicin is frequently incorporated in CBF-AML regimens, supported by a meta-analysis showing the greatest survival benefit in favorable cytogenetic groups, although real-world studies demonstrate treatment heterogeneity. Allogeneic hematopoietic-cell transplantation is not routinely used in first remission for patients with adequate response but may be considered when molecular response is unsatisfactory or disease recurs [23-25, 28, 29]. Quantitative reverse-transcription polymerase chain reaction for CBFB::MYH11 is recommended for molecular MRD assessment. Transcript reduction after induction/consolidation and serial re-emergence during surveillance correlate with relapse risk. Recent studies suggest that post-cycle-2 transcript levels may identify patients who benefit from altered post-remission strategies, but thresholds should be interpreted within the treatment protocol and assay framework [19-21, 26, 28, 29]. Differential diagnostic considerations AML with monocytic differentiation without a defining recurrent genetic abnormality would not explain the abnormal eosinophilic precursors, inv(16), and CBFB split signal. Myeloid/lymphoid neoplasms with eosinophilia and tyrosine-kinase fusions are relevant when eosinophilia is prominent and CBFB-directed studies are negative or discordant, but were not supported in this case. Chronic myeloid leukemia in blast phase may show splenomegaly, basophilia, left-shifted granulopoiesis, and harlequin cells; however, the absence of a documented chronic phase and the concordant inv(16)/CBFB findings favored de novo CBF-AML. Reactive eosinophilia cannot account for the clonal chromosome 16 abnormality or the high blast-equivalent burden [1, 2, 5, 30].

AML with inv(16) may show a diagnostically important abnormal eosinophilic component. In this case, coarse basophilic granules and a harlequin-type eosinophil provided the key morphologic clue, while karyotyping and CBFB break-apart FISH confirmed the diagnosis. Careful integration of morphology, flow cytometry, cytogenetics, and molecular testing when available is essential for accurate classification and appropriate measurable residual disease monitoring

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