Acute myeloid leukemia
acute myeloid leukemia blast cells bone marrow smear

High-magnification brightfield micrograph of a human bone marrow aspirate smear stained with Hematoxylin and Eosin, demonstrating dysplastic megakaryocytes in a hematopoietic background. The megakaryocytes exhibit atypical nuclear morphology, including multinucleation, irregular lobulation, and nuclear fragmentation, with variable cytoplasmic basophilia. Background cellularity shows concurrent dyserythropoiesis and dysplastic myeloid precursors consistent with a myelodysplastic spectrum. Overall architecture may be hypercellular or variably cellular, with scattered normal hematopoietic elements interspersed among abnormal cells. Features are most prominent in the megakaryocytic lineage, where dysplasia is a salient hallmark. The image illustrates morphologic criteria that support a diagnosis in the context of possible progression toward acute leukemia, and should be correlated with peripheral blood counts, marrow blast percentage, cytogenetic and molecular studies. Clinically, such dysplastic megakaryocytes are associated with cytopenias and splenomegaly, and approximately a fifth of patients with related myelodysplastic/myeloproliferative conditions progress to acute myeloid leukemia. This representation is valuable for educational, diagnostic, and research purposes, particularly in studies of megakaryocytic dysplasia, MDS/AML continuum, prognostication, and therapeutic planning focused on palliation and cytopenia management. Careful documentation of features and context enhances reproducibility, supports standardized reporting, and facilitates cross-institutional data sharing for outcome studies and biomarker-driven clinical trials.

Imaging modality: light microscopy of a hematopathology slide from a bone marrow aspirate smear. Stain: Hematoxylin and Eosin (H&E). Magnification: high-power field (~400x total; 40x objective with 10x ocular). Anatomical location: bone marrow within the medullary cavity (hematopoietic tissue). Visual features: sheets of immature blasts with high nuclear-to-cytoplasmic ratio, round to oval nuclei, fine chromatin, prominent nucleoli, and scant basophilic cytoplasm; increased cellularity with near-complete effacement of normal hematopoiesis; occasional mitotic figures; minimal cytoplasmic granularity; sparse residual neutrophils, erythroid precursors, and megakaryocytes. Pathologic interpretation: diffuse marrow infiltration by blasts, consistent with an acute leukemia until immunophenotyping and genetic studies delineate subtype. Diagnostic significance: morphologic hallmark of an acute hematologic malignancy; requires ancillary tests (flow cytometry, immunohistochemistry, cytogenetics/molecular studies) for lineage classification (myeloid vs lymphoid), prognosis, and treatment planning. Differential considerations: ALL (acute lymphoblastic leukemia), AML (acute myeloid leukemia), lymphoblastic lymphoma with marrow involvement, myelodysplastic syndrome with excess blasts, or nonhematopoietic marrow infiltration. Clinical correlation: commonly presents with cytopenias, fatigue, infections, and bleeding; pediatric ALL vs adult AML guidance; urgent hematology-oncology workup is indicated. Educational use: foundational blast morphology recognition, marrow infiltration patterns, and the need for confirmatory immunophenotyping. This image is valuable for training in blast morphology, differential diagnosis, and education in hematopathology.

This composite educational graphic illustrates the morphologic and immunophenotypic evolution of a secondary Acute Myeloid Leukemia (AML) case across four clinical stages: primary diagnosis, first relapse, second relapse, and post-anti-CLL1 CAR T-cell therapy. Panel A consists of Wright-Giemsa stained bone marrow aspirate smears. Early stages show dense populations of myeloblasts with high N:C ratios, fine chromatin, and nucleoli. The second relapse reveals increasing dysplasia, while the post-therapy image demonstrates hematopoietic recovery with mature leukocytes and a significant reduction in blast cells. Panels B and C present flow cytometric scatter plots utilizing two gating strategies: 'All Events' and 'Blast+E' (blasts and erythroid cells). Markers analyzed include CD45, Side Scatter (SSC), CD34, CD123, CD38, CD33, CD10, and CD19. Color-coded populations identify blasts (red), lymphocytes (green), monocytes (dark blue), neutrophils (orange), and erythrocytes (light blue). The plots track the lineage switch and immunophenotypic shifts, such as the emergence of myeloid markers (CD33, CD123) in later relapses and the subsequent elimination of the malignant blast population following targeted CAR T-cell therapy.

Imaging modality: Histopathology with brightfield microscopy of an H&E stained femoral bone lesion. The specimen shows a dense, cellular marrow‑like infiltrate occupying bone with disruption of normal trabecular architecture. Individual cells are small to medium in size with high nuclear‑to‑cytoplasmic ratio, finely dispersed chromatin, and prominent nucleoli, compatible with myeloblasts. The cell population forms diffuse sheets with scant cytoplasm and frequent mitotic figures. Invasion surrounds a central vascular channel, and occasional residual bone spicules may be seen, consistent with granulocytic sarcoma (myeloid sarcoma), an extramedullary manifestation of acute myeloid leukemia. In the clinical context of chronic myeloid leukemia in blast crisis, this lesion reflects leukemic infiltration of periosteal and marrow compartments, often signaling systemic progression. When integrated with immunophenotype and molecular studies, this tissue supports diagnosis within the AML/acute leukemia spectrum and guides therapy toward AML‑type chemotherapy and consideration of stem cell transplantation. The image is relevant to differential diagnoses such as lymphoma, Ewing sarcoma, and other small round blue cell tumors, especially when cytochemical stains are unavailable. This histopathologic finding emphasizes the importance of evaluating myeloid neoplasms for extramedullary disease in bone and its implications for prognosis, staging, and multidisciplinary management.
"acute myeloid leukemia"[MeSH Terms] AND treatment
"acute myeloid leukemia"[MeSH Terms] AND "targeted therapy"
| Category | Genetic Aberration | Prognosis |
|---|---|---|
| AML with t(8;21); RUNX1::RUNX1T1 | Core binding factor | Favorable |
| AML with inv(16)/t(16;16); CBFB::MYH11 | Core binding factor | Favorable |
| APL with t(15;17); PML::RARα | Very favorable | |
| AML with KMT2A (11q23) rearrangement | >130 partners | Poor |
| AML with mutated NPM1 | Favorable (if FLT3-ITD low) | |
| AML with biallelic CEBPA | Favorable | |
| AML with t(6;9); DEK-NUP214 | Very poor | |
| AML with inv(3)/t(3;3); GATA2/MECOM | Very poor | |
| Therapy-related AML | Prior chemo/XRT | Poor |
| AML, NOS (by differentiation) | Various | Variable |
| Risk Group | Genetic Features |
|---|---|
| Favorable | t(8;21); inv(16)/t(16;16); NPM1 mutated without FLT3-ITD or with FLT3-ITD^low; biallelic CEBPA |
| Intermediate | NPM1 mutated + FLT3-ITD^high; wild-type NPM1 without FLT3-ITD^low; t(9;11) |
| Adverse | t(6;9); inv(3)/t(3;3); t(v;11q23) KMT2A; monosomy 5/7; complex karyotype; TP53 mutation |
| Stain | Positive in |
|---|---|
| MPO (myeloperoxidase) | Myeloblasts |
| Sudan black B (SBB) | Myeloblasts |
| Chloroacetate esterase (CAE) | Granulocytic lineage |
| α-naphthyl acetate/butyrate esterase (NaF-inhibited) | Monocytic lineage |
| Marker | Lineage |
|---|---|
| CD34, CD117, HLA-DR | Immature AML |
| CD13, CD33 | Myeloid |
| CD14, CD15, CD11b | Monocytic |
| CD36, CD71, CD235a (glycophorin A) | Erythroid |
| CD41, CD61 | Megakaryocytic |
| MPO | Myeloid (most specific) |
| Target | Drug | Indication |
|---|---|---|
| FLT3 | Midostaurin (+ "7+3"), Gilteritinib (relapsed/refractory) | FLT3-mutated AML |
| IDH1 | Ivosidenib | IDH1-mutated AML |
| IDH2 | Enasidenib | IDH2-mutated AML |
| BCL-2 | Venetoclax + azacitidine/low-dose ara-C | Elderly/unfit patients |
| CD33 | Gemtuzumab ozogamicin | CD33+ AML |


